In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance thro...In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance through an innovative biomimetic coating technology for brain chronic implants.We hypothesized that the autologous origin of human brain mic rovascular endothelial cells(hBMECs)is the first requirement for the suitable coating to prevent the glial inflammato ry response trigge red by foreign neuroprosthetics.Therefo re,this study established a new procedure to preserve the in vitro viability of hBMECs isolated from gray and white matter specimens taken from neurosurge ry patients.Culturing adult hBMECs is generally considered a challenging task due to the difficult survival ex vivo and progressive reduction in proliferation of these cells.The addition of 10 nMβ-estradiol 17-acetate to the hBMEC culture medium was found to be an essential and discriminating factor promoting adhesion and proliferation both after isolation and thawing,suppo rting the well-known protective role played by estrogens on microvessels.In particular,β-estradiol 17-acetate was critical for both freshly isolated and thawed female-derived hBMECs,while it was not necessary for freshly isolated male-derived hBMECs;however,it did countera ct the decay in the viability of the latter after thawing.The tumo r-free hBMECs were thus cultured for up to 2 months and their growth efficiency was assessed befo re and after two periods of cryopreservation.Des pite the thermal stress,the hBMECs remained viable and suitable for re-freezing and storage for several months.This approach increasing in vitro viability of hBMECs opens new perspectives for the use of cryopreserved autologous hBMECs as biomimetic therapeutic tools,offering the potential to avoid additional surgical sampling for each patient.展开更多
AIM:To investigate the impact of 17β-estradiol on the collagen gels contraction(CGC)and inflammation induced by transforming growth factor(TGF)-βin human Tenon fibroblasts(HTFs).METHODS:HTFs were three-dimensionally...AIM:To investigate the impact of 17β-estradiol on the collagen gels contraction(CGC)and inflammation induced by transforming growth factor(TGF)-βin human Tenon fibroblasts(HTFs).METHODS:HTFs were three-dimensionally cultivated in type I collagen-generated gels with or without TGF-β(5 ng/mL),17β-estradiol(12.5 to 100μmol/L),or progesterone(12.5 to 100μmol/L).Then,the collagen gel diameter was determined to assess the contraction,and the development of stress fibers was analyzed using immunofluorescence staining.Immunoblot and gelatin zymography assays were used to analyze matrix metalloproteinases(MMPs)and tissue inhibitors of metalloproteinases(TIMPs)being released into culture supernatants.Enzyme-linked immunosorbent assay(ELISA)and reverse transcription-quantitative polymerase chain reaction(RT-PCR)were used to detect interleukin(IL)-6,monocyte chemoattractant proteins(MCP)-1,and vascular endothelial growth factor(VEGF)in HTFs at the translational and transcriptional levels.The phosphorylation levels of Sma-and Mad-related proteins(Smads),mitogen-activated protein kinases(MAPKs),and protein kinase B(AKT)were measured by immunoblotting.Statistical analysis was performed using either the Tukey-Kramer test or Student’s unpaired t-test to compare the various treatments.RESULTS:The CGC caused by TGF-βin HTFs was significantly inhibited by 17β-estradiol(25 to 100μmol/L),and a statistically significant difference was observed when comparing the normal control group with 17β-estradiol concentrations exceeding 25μmol/L(P<0.05).The suppressive impact of 17β-estradiol became evident 24h after administration and peaked at 72h(P<0.05),whereas progesterone had no impact.Moreover,17β-estradiol attenuated the formation of stress fibers,and the production of MMP-3 and MMP-1 in HTFs stimulated by TGF-β.The expression of MCP-1,IL-6,and VEGF mRNA and protein in HTFs were suppressed by 100μmol/L 17β-estradiol(P<0.01).Additionally,the phosphorylation of Smad2 Smad3,p38,and extracellular signal-regulated kinase(ERK)were downregulated(P<0.01).CONCLUSION:17β-estradiol significantly inhibits the CGC and inflammation caused by TGF-βin HTFs.This inhibition is likely related to the suppression of stress fibers,inhibition of MMPs,and attenuation of Smads and MAPK(ERK and p38)signaling.17β-estradiol may have potential clinical benefits in preventing scar development and inflammation in the conjunctiva.展开更多
17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body wei...17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body weight gain. This study aimed to better understand the interferences that could exist between 17β-estradiol, D2 receptors and the selection of carbohydrate, fat and protein consumption, as well as their consequences on body weight gain by using an animal model of the menopause. Ovariectomy exacerbates the consumption of foods rich in lipids. Thus confirming an inhibitory action of 17β-estradiol (E2) on the consumption of these types of foods. This consumption stimulates body weight gain, which is promoted by the high caloric content of these foods and not by the amount consumed. Our results showed a direct involvement of D2 receptors in food choice. This choice would be made according to the two (2) isoforms of the D2 receptors. The D2/BR isoform directs towards a high carbohydrate consumption, without causing a gain in body weight. While D2/SUL, promotes high fat food consumption, causing an increase in body weight. In women, 17β-estradiol modulates the activity ratio between these two D2 receptor isoforms to ensure energy and homeostatic balance, stabilizing food intake and body weight.展开更多
Estrogen plays an important role in regulating Sertoli cell number in the testis. The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured, immature boar Sertoli cells v...Estrogen plays an important role in regulating Sertoli cell number in the testis. The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured, immature boar Sertoli cells via the estrogen receptor β (ERβ) and the cAMP-extracellular signal-regulated kinase (ERK1/2) pathway. Low levels (10-10-10-8 mol L-1) of 17β-estradiol increased cell number, but high levels (10-7-10-6 mol L-1) decreased it (P〈0.05). Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol (10-6 mol L-l) (P〉0.05). The effects of 17β-estradiol (10-9 mol L-1) peaked at the first 24 h (P〈0.05). 17β-estradiol activated ERK1/2 from 5 min to 24 h, but the activiy of ERK1/2 began to decrease after 4 h. Both PD98059 and U0126, two ERK inhibitors, blocked cell division (P〈0.05). 17β-estradiol (10-10-10-6 mol L-1) dose-dependently increased cAMP production (P 〈 0.05), and both 17β-estradiol (10-9 mol L-1) and forskolin, which increases cAMP levels, induced cell proliferation and activated ERK1/2 (P〈 0.05). Rp-cAMP, an antagonist of cAMP, blocked this 17β-estradiol activity (P〈 0.05). Two estrogen receptor antagonists, ICI 182780 and ERβ antagonist (ERβAnt), reduced Sertoli cell number, cAMP production and ERK1/2 activation (P〈 0.05), but ERaAnt did not (P〉 0.05). Therefore, 17β- estradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.展开更多
Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases inc...Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases including cancer.Nonetheless this information,the design and execution of studies on endocrine disruptors are not yet cognizant that the specific actions of individual hormones often change with development and ageing,they may be different in males and females and may be mediated by different receptors isoforms expressed in different tissues or at different life stages.These statements are particularly true when assessing the hazard of endocrine disruptors against 17β-estradiol(E2)actions in that this hormone is crucial determinant of sexrelated differences in anatomical,physiological,and behavioral traits which characterize male and female physiology.Moreover,E2 is also involved in carcinogenesis.The oncogenic effects of E2 have been investigated extensively in breast and ovarian cancers where hormone-receptor modulators are now an integral part of targeted treatment.Little is known about the E2preventive signalling in colorectal cancer,although this disease is more common in men than women,the difference being more striking amongst pre-menopausal women and age-matched men.This review aims to dissect the role and action mechanisms of E2 in colorectal cancer evaluating the ability of estrogen disruptors(i.e.,xenoestrogens)in impair these E2 actions.Data discussed here lead to define the possible role of xenoestrogens in the impairment and/or activation of E2signals important for colorectal cancer prevention.展开更多
Aim: To explore whether the anti-tumor action of 17β-estradiol is enhanced by re-expression of the homeodomain transcription factor Nkx3.1 in PC3 human prostate cancer cells. Methods: PC3 cells were stably transfec...Aim: To explore whether the anti-tumor action of 17β-estradiol is enhanced by re-expression of the homeodomain transcription factor Nkx3.1 in PC3 human prostate cancer cells. Methods: PC3 cells were stably transfected with pcDNA3.1-Nkx3.1-His vector, which carries a full-length cDNA of human Nkx3.1. The PC3 cells stably transfected with vector pcDNA3.1 were set as a control. The expression of Nkx3.1 protein in the cells was confirmed by Western blot analysis. The effect of Nkx3.1 on cell proliferation of PC3 cells was examined with MTT assay. The antiproliferative and apoptotic effects of 17β-estradiol alone or in combination with Nkx3.1 were estimated on PC3 cells by using MTT growth tests and flow cytometric analyses. The expression of apoptosis-related proteins was analyzed using Western blotting. Results: The plasmid carrying Nkx3.1 gene induced high expression of Nkx3.1 protein in PC3 cells. The re-expression of exogenous Nkx3.1 did not cause a significant reduction in cellular proliferation, whereas the expression of Nkx3.1 enhanced the 17β-estradiol anti-proliferative effect in PC3 cells. Nkx3.1 expres- sion promoted 17β-estradiol-induced apoptosis of PC3 cells, as shown by analysis of Bcl-2, Bax, Caspase-3 and poly (ADP-ribose) polymerase expression. Conclusion: The present study demonstrates that re-expression of Nkx3.1 enhances 17β-estradiol anti-tumor action in PC3 human prostate cancer cells. The in vitro study suggests that re- expression of Nkx3.1 is worthy of further consideration as an adjuvant treatment of androgen independent prostate cancer with estrogen anti-tumor therapies.展开更多
Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were...Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were observed in vitro. The response of the muscle strips to estrogen after incubation with either actinomycin D (10μmol/L) or L-NAME (10μmol/L) were also evaluated. Inside-out mode of patch clamp in a single smooth muscle cell was applied to investigate the Maxi-K channel activities. Results: Estrogen caused a dose-dependent relaxation of the strips precontracted with norepinephrine. The maximal response was noted about 10 minutes after treatment. The estrogen-induced relaxation was prevented by neither actinomycin D nor L-NAME, suggesting that the response was not mediated by gene transcription or nitric oxide (NO). Application of 17β-estradiol increased the Maxi-K channel activities. Conclusion: 17β-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a non genomic and NO independent mechanism. 17β-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.展开更多
The efficacy of Endocrine Disrupting Compounds (EDCs), 17β-estradiol was tested on the fish Oreochromis niloticus in order to understand the intersex relationship of fish, in which sequential hermaphrodism can consis...The efficacy of Endocrine Disrupting Compounds (EDCs), 17β-estradiol was tested on the fish Oreochromis niloticus in order to understand the intersex relationship of fish, in which sequential hermaphrodism can consist of a male changing into a female (protandry) or a female changing into a male (protogyny). The fish were equally divided into 3 groups. The first group was the control group;the second and third groups were treated with 10 and 100 mg L-1 of 17β-estradiol, respectively, for 30 days. The overall result in this experiment had no significant effect on the growth parameters. Among the two treated groups, the low concentration group shows results similar to those of the control groups. The high concentration group shows changes to the male reproductive system with the appearance of the testis-ova present resulting in an intersex condition of the male gonads. With this experiment, it can be concluded that 17β-estradiol at high concentration reveals positive changes towards the male reproductive system of the fish, Oreochromis niloticus.展开更多
The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sol...The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sole ( Cynoglossus semilaevis ), 17β-estradiol (E2) can be used reportedly to induce the feminization of fi sh, although the detailed regulatory network remained elusive. We treated the tongue sole fry before sex diff erentiation with E2 (10 and 30 μg/L) to identify potential targets of E2 in Chinese tongue sole. The E2 treatment indeed induced genetic male fi sh sex-reversal to phenotypic female. Using an iTRAQ-based comparative proteomic analysis, 409 proteins that diff erentially expressed after E2 induction were identifi ed, including 259 up-regulated and 150 down-regulated proteins. Furthermore, 19 diff erentially expressed proteins identifi ed in the comparative proteomic analysis were selected to assess their transcription and eight of them exhibited the same tendency. Functions of the eight proteins included mainly nucleotide and protein binding. Interestingly, a far upstream element-binding protein 3-like isoform exhibited the signifi cant upregulation both at transcription and translation levels after E2 treatment. This work identifi ed a set of candidate proteins for E2 response and deepened our understanding of E2 regulatory mechanism.展开更多
The original version of this article unfortunately contained a mistake. The publication year in the header on the first page (p.1113) of this article was incorrect. The corrected publication year is given below:
Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2 (SKP2) plays a central role in mammalian cell cycle progression. The objective of this ...Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2 (SKP2) plays a central role in mammalian cell cycle progression. The objective of this study was to determine whether 17β-estradiol can regulate the expression of SKP2, and the Sertoli cell cycle, via estrogen receptor β (ERβ), the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) and extracellular signal-regulated kinase (ERK1/2) pathway. When cultured immature boar Sertoli cells were treated with 17β-estradiol, a time-dependent increase in SKP2 mRNA and protein level was observed by real-time PCR and Western blot, and 17β-estradiol activity peaked at 30 min. Treatment with ICI182780 and ERβ antagonist reduced 17β-estradiol-induced expression of SKP2 and proliferating cell nuclear antigen (PCNA), while increasing the protein concentration of p27kip1. However, the effect of ERa antagonist on these parameters was lower than that of ICI 182780 and ERβ. Forskolin had a similar effect as 17β-estradiol on the expression of SKP2, PCNA and p27kip1, Rp-cAMP, H-89 and U0126 treatment reduced 17β-estradiol-induced changes, while H-89 also inhibited ERK1/2 activation. Therefore, 17β-estradiol mainly regulates SKP2 mRNA and protein expression via ERβ-cAMP-PKA and ERK1/2 activation. SKP2 and PCNA expression were positively correlated, while increased SKP2 expression likely resulted in p27kip1 degradation.展开更多
The aim of this study was to compare serum 17β-estradiol of menopausal women with/without Oral Dryness (OD) feeling, and evaluate the re-lationship between serum 17β-estradiol and severity of OD feeling. A case-cont...The aim of this study was to compare serum 17β-estradiol of menopausal women with/without Oral Dryness (OD) feeling, and evaluate the re-lationship between serum 17β-estradiol and severity of OD feeling. A case-control study was carried out on 70 selected menopausal women aged 40 - 77 years with or without OD feeling (35 as case, 35 as control) conducted at the Clinic of Oral Medicine, Tehran University of Medical Sciences. Xerostomia inventory (XI) score was used as an index of OD feeling severity. The serum 17β-estradiol concentration was measured by an enzyme immunoassay kit (ELISA). Statistical analysis of Student’s t-test and Spearman correlation coefficient was used. The mean serum concentration of 17β-estradiol was significantly lower in case than control. There was a significant negative correlation between XI score and concentration of 17β-estradiol in menopausal women (r = –0.311, P = 0.004). It seems that there is a negatively slight correlation between OD feeling severity and serum 17β-estradiol in menopausal women.展开更多
The following article has been retracted due to the investigation of complaints received against it. The Editorial Board found that the first author published the paper without other authors’ consent and approval. Th...The following article has been retracted due to the investigation of complaints received against it. The Editorial Board found that the first author published the paper without other authors’ consent and approval. The scientific community takes a very strong view on this matter, and the OJOG treats such behavior seriously. This paper published in Vol. 3 No. 1, 105-110 (pages), 2013, has been removed from this site.展开更多
In this research, bottom water samples were collected from nature water. After cultivating and selecting, bacteria which could use (NH<sub>4</sub>)<sub>2</sub>SO<sub>4</sub> as the ...In this research, bottom water samples were collected from nature water. After cultivating and selecting, bacteria which could use (NH<sub>4</sub>)<sub>2</sub>SO<sub>4</sub> as the only nitrogen source had been selected. The bacteria were cultivated in BM cultures with 0, 0.1, 1, 10, 100 ng/L 17β-estradiol (E2), and the initial concentration of E2 is the only difference between cultures of each group. BM culture is a kind of bacteria culture with 100 mg/L of NH4-N as only nitrogen source. Every group’s N- NH<sub>4</sub><sup>+</sup>, N- NO<sub>3</sub><sup>-</sup>concentration and OD600 were measured. The result shows that compared with the control group, in which no E2 was added, the growth of heterotrophic nitrifying bacteria had been promoted when the concentration of E2 was in range of 1 - 100 ng/L. In addition, heterotrophic nitrifying bacteria’s growing speed has a positive correlation between the E2’s concentration. However, low concentration of E2 (like 0.1 ng/L), could inhibit the growth of heterotrophic nitrifying bacteria. Considering the impact of E2 on heterotrophic nitrifying bacteria, it is necessary to intensify the detection of E2 in the future.展开更多
The Electrochemical advanced oxidation method “Electro-Fenton” has been applied to remove 17β-estradiol (17β)- estra-1,3,5(10)-triéne-3,17-diol) in aqueous-acetonitrile mixture. This endocrine disrupting is a...The Electrochemical advanced oxidation method “Electro-Fenton” has been applied to remove 17β-estradiol (17β)- estra-1,3,5(10)-triéne-3,17-diol) in aqueous-acetonitrile mixture. This endocrine disrupting is a steroid hormone, releases from humans, animals and residual pharmaceuticals into the environmental water and usually causes suspected undesirable effects in aquatic organisms. The degradation of this organic compound by Electro-Fenton process was showed using a carbon felt cathode and platinum anode. The evolution of the concentration during treatment was followed up by high performance liquid chromatography (HPLC). The influence of operating conditions on the degradation of 17β-estradiol by Electro-Fenton step, such as initial concentration and catalyst concentration, has been investi- gated and discussed. We showed that the degradation reaction obeyed apparent first-order reaction kinetics, with absolute rate constant determined as 5.12 × 109 M–1 s–1 by competitive kinetics method taking Benzoic Acid as reference compound. The results confirm the efficiency of the Electro-Fenton process to degrade organic pollutant in aqueous-acetonitrile mixture.展开更多
Estradiol, or 17-β-estradiol (E2), the most potent naturally occurring estrogen, is involved in the hormone-immune system interaction in both mammals and fish. However, in vivo studies are largely limited, and little...Estradiol, or 17-β-estradiol (E2), the most potent naturally occurring estrogen, is involved in the hormone-immune system interaction in both mammals and fish. However, in vivo studies are largely limited, and little is known about whether E2 exerts similar effects on both female and male zebrafish (Danio rerio). Here, we show exposure of both sexes of D. rerio to 20 nmol/L E2 resulted in a significant increase in Vg1 expression, but caused little damage to the hepatocytes, suggesting that this is the optimum E2 concentration. Also, exposure to 20 nmol/L E2 for 20 days caused a marked increase in plasma IgM levels, but had little influence on the peripheral leukocyte density, providing the first evidence of a hormone-immune system interaction in this species.展开更多
基金supported by EnTimeMent H2020-FETPROACT-824160(to LF)。
文摘In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance through an innovative biomimetic coating technology for brain chronic implants.We hypothesized that the autologous origin of human brain mic rovascular endothelial cells(hBMECs)is the first requirement for the suitable coating to prevent the glial inflammato ry response trigge red by foreign neuroprosthetics.Therefo re,this study established a new procedure to preserve the in vitro viability of hBMECs isolated from gray and white matter specimens taken from neurosurge ry patients.Culturing adult hBMECs is generally considered a challenging task due to the difficult survival ex vivo and progressive reduction in proliferation of these cells.The addition of 10 nMβ-estradiol 17-acetate to the hBMEC culture medium was found to be an essential and discriminating factor promoting adhesion and proliferation both after isolation and thawing,suppo rting the well-known protective role played by estrogens on microvessels.In particular,β-estradiol 17-acetate was critical for both freshly isolated and thawed female-derived hBMECs,while it was not necessary for freshly isolated male-derived hBMECs;however,it did countera ct the decay in the viability of the latter after thawing.The tumo r-free hBMECs were thus cultured for up to 2 months and their growth efficiency was assessed befo re and after two periods of cryopreservation.Des pite the thermal stress,the hBMECs remained viable and suitable for re-freezing and storage for several months.This approach increasing in vitro viability of hBMECs opens new perspectives for the use of cryopreserved autologous hBMECs as biomimetic therapeutic tools,offering the potential to avoid additional surgical sampling for each patient.
基金Supported by the National Natural Science Foundation of China(No.81770889)Zhuhai Science and Technology Program(No.ZH22036201210134PWC).
文摘AIM:To investigate the impact of 17β-estradiol on the collagen gels contraction(CGC)and inflammation induced by transforming growth factor(TGF)-βin human Tenon fibroblasts(HTFs).METHODS:HTFs were three-dimensionally cultivated in type I collagen-generated gels with or without TGF-β(5 ng/mL),17β-estradiol(12.5 to 100μmol/L),or progesterone(12.5 to 100μmol/L).Then,the collagen gel diameter was determined to assess the contraction,and the development of stress fibers was analyzed using immunofluorescence staining.Immunoblot and gelatin zymography assays were used to analyze matrix metalloproteinases(MMPs)and tissue inhibitors of metalloproteinases(TIMPs)being released into culture supernatants.Enzyme-linked immunosorbent assay(ELISA)and reverse transcription-quantitative polymerase chain reaction(RT-PCR)were used to detect interleukin(IL)-6,monocyte chemoattractant proteins(MCP)-1,and vascular endothelial growth factor(VEGF)in HTFs at the translational and transcriptional levels.The phosphorylation levels of Sma-and Mad-related proteins(Smads),mitogen-activated protein kinases(MAPKs),and protein kinase B(AKT)were measured by immunoblotting.Statistical analysis was performed using either the Tukey-Kramer test or Student’s unpaired t-test to compare the various treatments.RESULTS:The CGC caused by TGF-βin HTFs was significantly inhibited by 17β-estradiol(25 to 100μmol/L),and a statistically significant difference was observed when comparing the normal control group with 17β-estradiol concentrations exceeding 25μmol/L(P<0.05).The suppressive impact of 17β-estradiol became evident 24h after administration and peaked at 72h(P<0.05),whereas progesterone had no impact.Moreover,17β-estradiol attenuated the formation of stress fibers,and the production of MMP-3 and MMP-1 in HTFs stimulated by TGF-β.The expression of MCP-1,IL-6,and VEGF mRNA and protein in HTFs were suppressed by 100μmol/L 17β-estradiol(P<0.01).Additionally,the phosphorylation of Smad2 Smad3,p38,and extracellular signal-regulated kinase(ERK)were downregulated(P<0.01).CONCLUSION:17β-estradiol significantly inhibits the CGC and inflammation caused by TGF-βin HTFs.This inhibition is likely related to the suppression of stress fibers,inhibition of MMPs,and attenuation of Smads and MAPK(ERK and p38)signaling.17β-estradiol may have potential clinical benefits in preventing scar development and inflammation in the conjunctiva.
文摘17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body weight gain. This study aimed to better understand the interferences that could exist between 17β-estradiol, D2 receptors and the selection of carbohydrate, fat and protein consumption, as well as their consequences on body weight gain by using an animal model of the menopause. Ovariectomy exacerbates the consumption of foods rich in lipids. Thus confirming an inhibitory action of 17β-estradiol (E2) on the consumption of these types of foods. This consumption stimulates body weight gain, which is promoted by the high caloric content of these foods and not by the amount consumed. Our results showed a direct involvement of D2 receptors in food choice. This choice would be made according to the two (2) isoforms of the D2 receptors. The D2/BR isoform directs towards a high carbohydrate consumption, without causing a gain in body weight. While D2/SUL, promotes high fat food consumption, causing an increase in body weight. In women, 17β-estradiol modulates the activity ratio between these two D2 receptor isoforms to ensure energy and homeostatic balance, stabilizing food intake and body weight.
基金supported by the National Natural Science Foundation of China(30270955)the Foundamental Research Funds for the Central Universities,China(XDJK2009B035)
文摘Estrogen plays an important role in regulating Sertoli cell number in the testis. The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured, immature boar Sertoli cells via the estrogen receptor β (ERβ) and the cAMP-extracellular signal-regulated kinase (ERK1/2) pathway. Low levels (10-10-10-8 mol L-1) of 17β-estradiol increased cell number, but high levels (10-7-10-6 mol L-1) decreased it (P〈0.05). Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol (10-6 mol L-l) (P〉0.05). The effects of 17β-estradiol (10-9 mol L-1) peaked at the first 24 h (P〈0.05). 17β-estradiol activated ERK1/2 from 5 min to 24 h, but the activiy of ERK1/2 began to decrease after 4 h. Both PD98059 and U0126, two ERK inhibitors, blocked cell division (P〈0.05). 17β-estradiol (10-10-10-6 mol L-1) dose-dependently increased cAMP production (P 〈 0.05), and both 17β-estradiol (10-9 mol L-1) and forskolin, which increases cAMP levels, induced cell proliferation and activated ERK1/2 (P〈 0.05). Rp-cAMP, an antagonist of cAMP, blocked this 17β-estradiol activity (P〈 0.05). Two estrogen receptor antagonists, ICI 182780 and ERβ antagonist (ERβAnt), reduced Sertoli cell number, cAMP production and ERK1/2 activation (P〈 0.05), but ERaAnt did not (P〉 0.05). Therefore, 17β- estradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.
文摘Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases including cancer.Nonetheless this information,the design and execution of studies on endocrine disruptors are not yet cognizant that the specific actions of individual hormones often change with development and ageing,they may be different in males and females and may be mediated by different receptors isoforms expressed in different tissues or at different life stages.These statements are particularly true when assessing the hazard of endocrine disruptors against 17β-estradiol(E2)actions in that this hormone is crucial determinant of sexrelated differences in anatomical,physiological,and behavioral traits which characterize male and female physiology.Moreover,E2 is also involved in carcinogenesis.The oncogenic effects of E2 have been investigated extensively in breast and ovarian cancers where hormone-receptor modulators are now an integral part of targeted treatment.Little is known about the E2preventive signalling in colorectal cancer,although this disease is more common in men than women,the difference being more striking amongst pre-menopausal women and age-matched men.This review aims to dissect the role and action mechanisms of E2 in colorectal cancer evaluating the ability of estrogen disruptors(i.e.,xenoestrogens)in impair these E2 actions.Data discussed here lead to define the possible role of xenoestrogens in the impairment and/or activation of E2signals important for colorectal cancer prevention.
文摘Aim: To explore whether the anti-tumor action of 17β-estradiol is enhanced by re-expression of the homeodomain transcription factor Nkx3.1 in PC3 human prostate cancer cells. Methods: PC3 cells were stably transfected with pcDNA3.1-Nkx3.1-His vector, which carries a full-length cDNA of human Nkx3.1. The PC3 cells stably transfected with vector pcDNA3.1 were set as a control. The expression of Nkx3.1 protein in the cells was confirmed by Western blot analysis. The effect of Nkx3.1 on cell proliferation of PC3 cells was examined with MTT assay. The antiproliferative and apoptotic effects of 17β-estradiol alone or in combination with Nkx3.1 were estimated on PC3 cells by using MTT growth tests and flow cytometric analyses. The expression of apoptosis-related proteins was analyzed using Western blotting. Results: The plasmid carrying Nkx3.1 gene induced high expression of Nkx3.1 protein in PC3 cells. The re-expression of exogenous Nkx3.1 did not cause a significant reduction in cellular proliferation, whereas the expression of Nkx3.1 enhanced the 17β-estradiol anti-proliferative effect in PC3 cells. Nkx3.1 expres- sion promoted 17β-estradiol-induced apoptosis of PC3 cells, as shown by analysis of Bcl-2, Bax, Caspase-3 and poly (ADP-ribose) polymerase expression. Conclusion: The present study demonstrates that re-expression of Nkx3.1 enhances 17β-estradiol anti-tumor action in PC3 human prostate cancer cells. The in vitro study suggests that re- expression of Nkx3.1 is worthy of further consideration as an adjuvant treatment of androgen independent prostate cancer with estrogen anti-tumor therapies.
文摘Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were observed in vitro. The response of the muscle strips to estrogen after incubation with either actinomycin D (10μmol/L) or L-NAME (10μmol/L) were also evaluated. Inside-out mode of patch clamp in a single smooth muscle cell was applied to investigate the Maxi-K channel activities. Results: Estrogen caused a dose-dependent relaxation of the strips precontracted with norepinephrine. The maximal response was noted about 10 minutes after treatment. The estrogen-induced relaxation was prevented by neither actinomycin D nor L-NAME, suggesting that the response was not mediated by gene transcription or nitric oxide (NO). Application of 17β-estradiol increased the Maxi-K channel activities. Conclusion: 17β-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a non genomic and NO independent mechanism. 17β-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.
文摘The efficacy of Endocrine Disrupting Compounds (EDCs), 17β-estradiol was tested on the fish Oreochromis niloticus in order to understand the intersex relationship of fish, in which sequential hermaphrodism can consist of a male changing into a female (protandry) or a female changing into a male (protogyny). The fish were equally divided into 3 groups. The first group was the control group;the second and third groups were treated with 10 and 100 mg L-1 of 17β-estradiol, respectively, for 30 days. The overall result in this experiment had no significant effect on the growth parameters. Among the two treated groups, the low concentration group shows results similar to those of the control groups. The high concentration group shows changes to the male reproductive system with the appearance of the testis-ova present resulting in an intersex condition of the male gonads. With this experiment, it can be concluded that 17β-estradiol at high concentration reveals positive changes towards the male reproductive system of the fish, Oreochromis niloticus.
基金Supported by the Natural Science Foundation of Shandong Province(No.ZR2014CQ053)the National Natural Science Foundation of China(No.31402293)the Taishan Scholar Climbing Program of Shandong Province,China
文摘The phenomenon of sex dimorphism prevails among many fi sh species. It has attracted the general research interest due to its close relationship to fi sh growth and thus aquaculture productivity. In Chinese tongue sole ( Cynoglossus semilaevis ), 17β-estradiol (E2) can be used reportedly to induce the feminization of fi sh, although the detailed regulatory network remained elusive. We treated the tongue sole fry before sex diff erentiation with E2 (10 and 30 μg/L) to identify potential targets of E2 in Chinese tongue sole. The E2 treatment indeed induced genetic male fi sh sex-reversal to phenotypic female. Using an iTRAQ-based comparative proteomic analysis, 409 proteins that diff erentially expressed after E2 induction were identifi ed, including 259 up-regulated and 150 down-regulated proteins. Furthermore, 19 diff erentially expressed proteins identifi ed in the comparative proteomic analysis were selected to assess their transcription and eight of them exhibited the same tendency. Functions of the eight proteins included mainly nucleotide and protein binding. Interestingly, a far upstream element-binding protein 3-like isoform exhibited the signifi cant upregulation both at transcription and translation levels after E2 treatment. This work identifi ed a set of candidate proteins for E2 response and deepened our understanding of E2 regulatory mechanism.
文摘The original version of this article unfortunately contained a mistake. The publication year in the header on the first page (p.1113) of this article was incorrect. The corrected publication year is given below:
基金grants from the National Natural Science Foundation of China(31072183)the Fundamental Research Funds for the Central Universities,China(XDJK2009B035)
文摘Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2 (SKP2) plays a central role in mammalian cell cycle progression. The objective of this study was to determine whether 17β-estradiol can regulate the expression of SKP2, and the Sertoli cell cycle, via estrogen receptor β (ERβ), the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) and extracellular signal-regulated kinase (ERK1/2) pathway. When cultured immature boar Sertoli cells were treated with 17β-estradiol, a time-dependent increase in SKP2 mRNA and protein level was observed by real-time PCR and Western blot, and 17β-estradiol activity peaked at 30 min. Treatment with ICI182780 and ERβ antagonist reduced 17β-estradiol-induced expression of SKP2 and proliferating cell nuclear antigen (PCNA), while increasing the protein concentration of p27kip1. However, the effect of ERa antagonist on these parameters was lower than that of ICI 182780 and ERβ. Forskolin had a similar effect as 17β-estradiol on the expression of SKP2, PCNA and p27kip1, Rp-cAMP, H-89 and U0126 treatment reduced 17β-estradiol-induced changes, while H-89 also inhibited ERK1/2 activation. Therefore, 17β-estradiol mainly regulates SKP2 mRNA and protein expression via ERβ-cAMP-PKA and ERK1/2 activation. SKP2 and PCNA expression were positively correlated, while increased SKP2 expression likely resulted in p27kip1 degradation.
文摘The aim of this study was to compare serum 17β-estradiol of menopausal women with/without Oral Dryness (OD) feeling, and evaluate the re-lationship between serum 17β-estradiol and severity of OD feeling. A case-control study was carried out on 70 selected menopausal women aged 40 - 77 years with or without OD feeling (35 as case, 35 as control) conducted at the Clinic of Oral Medicine, Tehran University of Medical Sciences. Xerostomia inventory (XI) score was used as an index of OD feeling severity. The serum 17β-estradiol concentration was measured by an enzyme immunoassay kit (ELISA). Statistical analysis of Student’s t-test and Spearman correlation coefficient was used. The mean serum concentration of 17β-estradiol was significantly lower in case than control. There was a significant negative correlation between XI score and concentration of 17β-estradiol in menopausal women (r = –0.311, P = 0.004). It seems that there is a negatively slight correlation between OD feeling severity and serum 17β-estradiol in menopausal women.
文摘The following article has been retracted due to the investigation of complaints received against it. The Editorial Board found that the first author published the paper without other authors’ consent and approval. The scientific community takes a very strong view on this matter, and the OJOG treats such behavior seriously. This paper published in Vol. 3 No. 1, 105-110 (pages), 2013, has been removed from this site.
文摘In this research, bottom water samples were collected from nature water. After cultivating and selecting, bacteria which could use (NH<sub>4</sub>)<sub>2</sub>SO<sub>4</sub> as the only nitrogen source had been selected. The bacteria were cultivated in BM cultures with 0, 0.1, 1, 10, 100 ng/L 17β-estradiol (E2), and the initial concentration of E2 is the only difference between cultures of each group. BM culture is a kind of bacteria culture with 100 mg/L of NH4-N as only nitrogen source. Every group’s N- NH<sub>4</sub><sup>+</sup>, N- NO<sub>3</sub><sup>-</sup>concentration and OD600 were measured. The result shows that compared with the control group, in which no E2 was added, the growth of heterotrophic nitrifying bacteria had been promoted when the concentration of E2 was in range of 1 - 100 ng/L. In addition, heterotrophic nitrifying bacteria’s growing speed has a positive correlation between the E2’s concentration. However, low concentration of E2 (like 0.1 ng/L), could inhibit the growth of heterotrophic nitrifying bacteria. Considering the impact of E2 on heterotrophic nitrifying bacteria, it is necessary to intensify the detection of E2 in the future.
文摘The Electrochemical advanced oxidation method “Electro-Fenton” has been applied to remove 17β-estradiol (17β)- estra-1,3,5(10)-triéne-3,17-diol) in aqueous-acetonitrile mixture. This endocrine disrupting is a steroid hormone, releases from humans, animals and residual pharmaceuticals into the environmental water and usually causes suspected undesirable effects in aquatic organisms. The degradation of this organic compound by Electro-Fenton process was showed using a carbon felt cathode and platinum anode. The evolution of the concentration during treatment was followed up by high performance liquid chromatography (HPLC). The influence of operating conditions on the degradation of 17β-estradiol by Electro-Fenton step, such as initial concentration and catalyst concentration, has been investi- gated and discussed. We showed that the degradation reaction obeyed apparent first-order reaction kinetics, with absolute rate constant determined as 5.12 × 109 M–1 s–1 by competitive kinetics method taking Benzoic Acid as reference compound. The results confirm the efficiency of the Electro-Fenton process to degrade organic pollutant in aqueous-acetonitrile mixture.
基金Supported by the Natural Science Foundation of Shandong Province (No. 2007ZRB02238)the Natural Science Foundation of Qingdao Municipality (No. 06-2-2-15-jch)
文摘Estradiol, or 17-β-estradiol (E2), the most potent naturally occurring estrogen, is involved in the hormone-immune system interaction in both mammals and fish. However, in vivo studies are largely limited, and little is known about whether E2 exerts similar effects on both female and male zebrafish (Danio rerio). Here, we show exposure of both sexes of D. rerio to 20 nmol/L E2 resulted in a significant increase in Vg1 expression, but caused little damage to the hepatocytes, suggesting that this is the optimum E2 concentration. Also, exposure to 20 nmol/L E2 for 20 days caused a marked increase in plasma IgM levels, but had little influence on the peripheral leukocyte density, providing the first evidence of a hormone-immune system interaction in this species.