BACKGROUND Visceral obesity is increasingly prevalent among adolescents and young adults and is commonly recognized as a risk factor for type 2 diabetes.Estrogen[17β-estradiol(E2)]is known to offer protection against...BACKGROUND Visceral obesity is increasingly prevalent among adolescents and young adults and is commonly recognized as a risk factor for type 2 diabetes.Estrogen[17β-estradiol(E2)]is known to offer protection against obesity via diverse me-chanisms,while its specific effects on visceral adipose tissue(VAT)remain to be fully elucidated.AIM To investigate the impact of E2 on the gene expression profile within VAT of a mouse model of prediabetes.METHODS Metabolic parameters were collected,encompassing body weight,weights of visceral and subcutaneous adipose tissues(VAT and SAT),random blood glucose levels,glucose tolerance,insulin tolerance,and overall body composition.The gene expression profiles of VAT were quantified utilizing the Whole Mouse Genome Oligo Microarray and subsequently analyzed through Agilent Feature Extraction software.Functional and pathway analyses were conducted employing Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses,respectively.RESULTS Feeding a high-fat diet(HFD)moderately increased the weights of both VAT and SAT,but this increase was mitigated by the protective effect of endogenous E2.Conversely,ovariectomy(OVX)led to a significant increase in VAT weight and the VAT/SAT weight ratio,and this increase was also reversed with E2 treatment.Notably,OVX diminished the expression of genes involved in lipid metabolism compared to HFD feeding alone,signaling a widespread reduction in lipid metabolic activity,which was completely counteracted by E2 adminis-tration.This study provides a comprehensive insight into E2's local and direct protective effects against visceral adiposity in VAT at the gene level.CONCLUSION In conclusion,the present study demonstrated that the HFD-induced over-nutritional challenge disrupted the gene expression profile of visceral fat,leading to a universally decreased lipid metabolic status in E2 deficient mice.E2 treatment effectively reversed this condition,shedding light on the mechanistic role and therapeutic potential of E2 in combating visceral obesity.展开更多
11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and type 2 (11β-HSD2) are expressed in rat testis, where they regulate the local concentrations of glucocorticoids. Here, we investigated the expression and lo...11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and type 2 (11β-HSD2) are expressed in rat testis, where they regulate the local concentrations of glucocorticoids. Here, we investigated the expression and localization of 11β-HSD in rat testis during postnatal development, and the regulation of these genes by luteinizing hormone (LH) and androgens, mRNA and protein levels were analyzed by quantitative real-time-polymerase chain reaction and western blotting, respectively, in testes collected from rats at postnatal day (PND) 7, 14, 21, 35, and 90, and from rats treated with LH, 7α.methyl-19-nortestosterone (MENT) and testosterone at PND 21 and PND 90. Immunohistochemical staining was used to identify the localization of the 11β-HSD in rat testis at PND 7, 14, and 90. We found that 11β-HSD1 expression was restricted to the interstitial areas, and that its levels increased during rat testis development. In contrast, whereas 11β-HSD2 was expressed in both the interstitial areas and seminiferous tubules at PND 7, it was present only in the interstitial areas at PND 90, and its levels declined during testicular development. Moreover, 11β-HSD1 mRNA was induced by LH in both the PND 21 and 90 testes and by MENT at PND 21, whereas 11β-HSD2 mRNA was induced by testosterone and MENT in the PND 21 testis and by LH in the PND 90 testis. In conclusion, our study indicates that the 11β-HSD1 and 11β-HSD2 genes have distinct patterns of spatiotemporal expression and hormonal regulation during postnatal development of the rat testis.展开更多
AIM:To explore the effect of miR-184 and miR-205 on the proliferation and metastasis of conjunctival mucosa associated lymphoid tissue(MALT)lymphoma.METHODS:Tissue of tumor and adjacent normal control from 5 patients ...AIM:To explore the effect of miR-184 and miR-205 on the proliferation and metastasis of conjunctival mucosa associated lymphoid tissue(MALT)lymphoma.METHODS:Tissue of tumor and adjacent normal control from 5 patients with conjunctival MALT was included.RPMI8226 cell line was selected to verify the effect of mi RNAs in B cells.The function of micro RNA on the RPMI8226 cell apoptosis,migration and invasion was evaluated by apoptosis assay and Transwell assay.The m RNA and protein expression were examined by quantitative RT-PCR and Western blotting.The effect of micro RNA on regulation of downstream gene expression was evaluated by luciferase report assay.RESULTS:A decreased level of miR-184 and miR-205 was observed in MALT lymphoma tissue.Exogenous miR-184 and miR-205 analogues promoted apoptosis,and inhibited the survival,migration,and invasion of RPMI8226 cells.miR-184 and miR-205 inhibitor reversed the process.The RNA and protein level of Ras L10 B and TNFAIP8 were downregulated in MALT lymphoma tissue.The exogenous of miR-184 and miR-205 promoted the expression of Ras L10 B and TNFAIP8.Meanwhile,inhibition of miR-184 and miR-205 repressed the expression of target gene,Ras L10 B and TNFAIP8.CONCLUSION:miR-184 and miR-205 suppresses the tumorigenesis of conjunctival MALT lymphoma through regulating Ras L10 B and TNFAIP8.展开更多
Pseudorabies,also known as Aujeszky's disease,is one of the most economically important viral diseases in pigs and is lethal to other susceptible animals(Ren et al.2020).The causative agent,pseudorabies virus(PRV)...Pseudorabies,also known as Aujeszky's disease,is one of the most economically important viral diseases in pigs and is lethal to other susceptible animals(Ren et al.2020).The causative agent,pseudorabies virus(PRV),is an enveloped virus with a large double-stranded DNA genome encoding at least 70 proteins(Wong et al.2019).PRV belongs to the family Herpesviridae,subfamily Alphaherpesvirinae,genus Varicellovirus and infects multiple animals,such as pigs,dogs,cats,rabbits,cattle,sheep,goats,minks.展开更多
Dear Editor, 46,XY disorder of sex development (DSD) is characterized by a female phenotype in an individual with a normal 46,XY karyotype.1 The clinical phenotTpe of 46,XY DSD is characterized by bilateral undesce...Dear Editor, 46,XY disorder of sex development (DSD) is characterized by a female phenotype in an individual with a normal 46,XY karyotype.1 The clinical phenotTpe of 46,XY DSD is characterized by bilateral undescended testes and a normal female appearance, including breasts, female external genitalia, and other secondary sex characteristics, but the absence of a uterus or ovaries.2 Development of the male external genitalia in the fetal period depends on the biosynthesis of testosterone (T), the conversion ofT into dihydrotestosterone (DHT) by steroid 5α-reductase type 2 (SRD5A2), and the response of functionally active androgen receptors in genital tissues) The disruption of any of these stages will block the differentiation of internal and external genitalia and cause 46,XY DSD.展开更多
基金Supported by National Natural Science Foundation of China,No.81270901 and No.81970672.
文摘BACKGROUND Visceral obesity is increasingly prevalent among adolescents and young adults and is commonly recognized as a risk factor for type 2 diabetes.Estrogen[17β-estradiol(E2)]is known to offer protection against obesity via diverse me-chanisms,while its specific effects on visceral adipose tissue(VAT)remain to be fully elucidated.AIM To investigate the impact of E2 on the gene expression profile within VAT of a mouse model of prediabetes.METHODS Metabolic parameters were collected,encompassing body weight,weights of visceral and subcutaneous adipose tissues(VAT and SAT),random blood glucose levels,glucose tolerance,insulin tolerance,and overall body composition.The gene expression profiles of VAT were quantified utilizing the Whole Mouse Genome Oligo Microarray and subsequently analyzed through Agilent Feature Extraction software.Functional and pathway analyses were conducted employing Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses,respectively.RESULTS Feeding a high-fat diet(HFD)moderately increased the weights of both VAT and SAT,but this increase was mitigated by the protective effect of endogenous E2.Conversely,ovariectomy(OVX)led to a significant increase in VAT weight and the VAT/SAT weight ratio,and this increase was also reversed with E2 treatment.Notably,OVX diminished the expression of genes involved in lipid metabolism compared to HFD feeding alone,signaling a widespread reduction in lipid metabolic activity,which was completely counteracted by E2 adminis-tration.This study provides a comprehensive insight into E2's local and direct protective effects against visceral adiposity in VAT at the gene level.CONCLUSION In conclusion,the present study demonstrated that the HFD-induced over-nutritional challenge disrupted the gene expression profile of visceral fat,leading to a universally decreased lipid metabolic status in E2 deficient mice.E2 treatment effectively reversed this condition,shedding light on the mechanistic role and therapeutic potential of E2 in combating visceral obesity.
文摘11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and type 2 (11β-HSD2) are expressed in rat testis, where they regulate the local concentrations of glucocorticoids. Here, we investigated the expression and localization of 11β-HSD in rat testis during postnatal development, and the regulation of these genes by luteinizing hormone (LH) and androgens, mRNA and protein levels were analyzed by quantitative real-time-polymerase chain reaction and western blotting, respectively, in testes collected from rats at postnatal day (PND) 7, 14, 21, 35, and 90, and from rats treated with LH, 7α.methyl-19-nortestosterone (MENT) and testosterone at PND 21 and PND 90. Immunohistochemical staining was used to identify the localization of the 11β-HSD in rat testis at PND 7, 14, and 90. We found that 11β-HSD1 expression was restricted to the interstitial areas, and that its levels increased during rat testis development. In contrast, whereas 11β-HSD2 was expressed in both the interstitial areas and seminiferous tubules at PND 7, it was present only in the interstitial areas at PND 90, and its levels declined during testicular development. Moreover, 11β-HSD1 mRNA was induced by LH in both the PND 21 and 90 testes and by MENT at PND 21, whereas 11β-HSD2 mRNA was induced by testosterone and MENT in the PND 21 testis and by LH in the PND 90 testis. In conclusion, our study indicates that the 11β-HSD1 and 11β-HSD2 genes have distinct patterns of spatiotemporal expression and hormonal regulation during postnatal development of the rat testis.
文摘AIM:To explore the effect of miR-184 and miR-205 on the proliferation and metastasis of conjunctival mucosa associated lymphoid tissue(MALT)lymphoma.METHODS:Tissue of tumor and adjacent normal control from 5 patients with conjunctival MALT was included.RPMI8226 cell line was selected to verify the effect of mi RNAs in B cells.The function of micro RNA on the RPMI8226 cell apoptosis,migration and invasion was evaluated by apoptosis assay and Transwell assay.The m RNA and protein expression were examined by quantitative RT-PCR and Western blotting.The effect of micro RNA on regulation of downstream gene expression was evaluated by luciferase report assay.RESULTS:A decreased level of miR-184 and miR-205 was observed in MALT lymphoma tissue.Exogenous miR-184 and miR-205 analogues promoted apoptosis,and inhibited the survival,migration,and invasion of RPMI8226 cells.miR-184 and miR-205 inhibitor reversed the process.The RNA and protein level of Ras L10 B and TNFAIP8 were downregulated in MALT lymphoma tissue.The exogenous of miR-184 and miR-205 promoted the expression of Ras L10 B and TNFAIP8.Meanwhile,inhibition of miR-184 and miR-205 repressed the expression of target gene,Ras L10 B and TNFAIP8.CONCLUSION:miR-184 and miR-205 suppresses the tumorigenesis of conjunctival MALT lymphoma through regulating Ras L10 B and TNFAIP8.
基金This work was supported by the National Natural Science Funds of China(31902281)the Science-Technology Foundation for Outstanding Young Scientists of Henan Academy of Agricultural Sciences(2020YQ15).
文摘Pseudorabies,also known as Aujeszky's disease,is one of the most economically important viral diseases in pigs and is lethal to other susceptible animals(Ren et al.2020).The causative agent,pseudorabies virus(PRV),is an enveloped virus with a large double-stranded DNA genome encoding at least 70 proteins(Wong et al.2019).PRV belongs to the family Herpesviridae,subfamily Alphaherpesvirinae,genus Varicellovirus and infects multiple animals,such as pigs,dogs,cats,rabbits,cattle,sheep,goats,minks.
文摘Dear Editor, 46,XY disorder of sex development (DSD) is characterized by a female phenotype in an individual with a normal 46,XY karyotype.1 The clinical phenotTpe of 46,XY DSD is characterized by bilateral undescended testes and a normal female appearance, including breasts, female external genitalia, and other secondary sex characteristics, but the absence of a uterus or ovaries.2 Development of the male external genitalia in the fetal period depends on the biosynthesis of testosterone (T), the conversion ofT into dihydrotestosterone (DHT) by steroid 5α-reductase type 2 (SRD5A2), and the response of functionally active androgen receptors in genital tissues) The disruption of any of these stages will block the differentiation of internal and external genitalia and cause 46,XY DSD.