Pulmonary surfactant is a lipid-protein complex secreted by alveolar typeⅡepithelial cells and is essential for the maintenance of the delicate structure of mammalian alveoli to promote efficient gas exchange across ...Pulmonary surfactant is a lipid-protein complex secreted by alveolar typeⅡepithelial cells and is essential for the maintenance of the delicate structure of mammalian alveoli to promote efficient gas exchange across the air-liquid barrier.The Golgi apparatus plays an important role in pulmonary surfactant modification and secretory trafficking.However,the physiological function of the Golgi apparatus in the transport of pulmonary surfactants is unclear.In the present study,deletion of GM130,which encodes for a matrix protein of the cis-Golgi cisternae,was shown to induce the disruption of the Golgi structure leading to impaired secretion of lung surfactant proteins and lipids.Specifically,the results of in vitro and in vivo analysis indicated that the loss of GM130 resulted in trapping of Sftpa in the endoplasmic reticulum,Sftpb and Sftpc accumulation in the Golgi apparatus,and an increase in the compensatory secretion of Sftpd.Moreover,global and epithelial-specific GM130 knockout in mice resulted in an enlargement of alveolar airspace and an increase in alveolar epithelial autophagy;however,surfactant repletion partially rescued the enlarged airspace defects in GM130-deficient mice.Therefore,our results demonstrate that GM130 and the mammalian Golgi apparatus play a critical role in the control of surfactant protein secretion in pulmonary epithelial cells.展开更多
Summary: The pathogenesis of hyperoxia lung injury and the mechanism of amygdalin on type 2 alveolar epithelial cells (AEC2) isolated from premature rat lungs in vitro were investigated. AEC2 were obtained by primary ...Summary: The pathogenesis of hyperoxia lung injury and the mechanism of amygdalin on type 2 alveolar epithelial cells (AEC2) isolated from premature rat lungs in vitro were investigated. AEC2 were obtained by primary culture from 20-days fetal rat lung and hyperoxia-exposed cell model was established. Cell proliferating viability was examined by MTT assay after treatment of amygdalin at various concentrations. DNA content and the proliferating cell nuclear antigen (PCNA) protein expression of AEC2 were measured by using flow cytometry and immunocytochemistry respectively after 24 h of hyperoxia exposure or amygdalin treatment. The results showed that hyperoxia inhibited the proliferation and decreased PCNA protein expression in AEC2 of premature rat in vitro. Amygdalin at the concentration range of 50-200 μmol/L stimulated the proliferation of AEC2 in a dose-dependent manner, however, 400 μmol/L amygdalin inhibited the proliferation of AEC2. Amygdalin at the concentration of 200 μmol/L played its best role in facilitating proliferation of AEC2s in vitro and could partially ameliorated the changes of proliferation in hyperoxia exposed AEC2 of premature rat. It has been suggested that hyperoxia inhibited the proliferation of AEC2s of premature rat, which may contribute to hyperoxia lung injury. Amygdalin may play partial protective role in hyperoxia-induced lung injury.展开更多
To establish a better method of primary culture for alveolar epithelial type Ⅱ cells （AEC Ⅱ ） and to study its bionomics, alveolar epithelial type Ⅱ cells were isolated by digestion with trypsin and collagenase, ...To establish a better method of primary culture for alveolar epithelial type Ⅱ cells （AEC Ⅱ ） and to study its bionomics, alveolar epithelial type Ⅱ cells were isolated by digestion with trypsin and collagenase, which were then purified by plated into culture flask coated with rat immunoglobulin （i The purified AEC Ⅱ were identified by alkaline phosphatase staining, electron mi- croscopy, immunocytochemical staining of pulmonary surfactant protein A （SPA）. The SPA expression and transfection characteristics were compared with those of A549 cell line. The results showed that AEC Ⅱ could be isolated by digestion with trysin and collagenase and purified by adhesive purification by using IgG, with a yield of about 2-3 × 10^7, and a purity of about 75%-84 %. Cells could be quickly identified with AKP staining. AEC Ⅱ were different from A549 cell line in terms of SPA expression and transfection characteristics. It is concluded that adhesive purification with IgG can improve the purity of AEC Ⅱ, and AKP staining is simple in cell identification. AEC Ⅱ can not be completely replaced by A549 cells in some studies because the differences between them, such as SPA expression.展开更多
Objective:To investigate the effects of mechanical stretching and lipopolysaccharide(LPS) on the early apoptosis and IL-8 production of alveolar epithelial type II cells A549.Methods:The experimental matrix consisted ...Objective:To investigate the effects of mechanical stretching and lipopolysaccharide(LPS) on the early apoptosis and IL-8 production of alveolar epithelial type II cells A549.Methods:The experimental matrix consisted of three integrated studies.In the first study,A549 cells were subjected to different stretching strain frequency and duration time to see the effects on the early apoptosis.In the second study,A549 cells were subjected to mechanical stretch(13%4 h, 0.3 Hz) and LPS(1 or 100 ng/mL) to see whether mechanical strain and LPS also have an addictive effect on the early apoptosis.In the third study to investigate whether this addictive effect could be induced by LPS and mechanical stretch on IL-8 production,A549 cells were subjected to LPS(100 ng/mL) and mechanical strain(13%.0.3 Hz,4 h).Real time PCR and enzyme linked immunosorbent assay were used to measure mRN A and protein level of IL-8.The early apoptosis was detected by flow cytometry.Results:Mechanical stretch induced the early apoptosis in a force and frequency and time-dependent manner.In the presence of LPS,mechanical stretch enhanced LPS-induced early apoptosis,especially in 100 ng/mL IPS group compared with 1 ng/ mL LPS and the control group.Mechanical stretch increased IL-8 production and enhanced LPS-induced IL-8 screation both in mRNA and protein levels.Conclusions:Mechanical stretch can induce the early apoptosis and IL-8 secretion.Mechanical stretch and LPS have an addictive effect on the early apoptosis and IL-8 production in alveolar type 2 cells,which is one of the mechanisms of ventilator-induced lung injury.展开更多
Objective To explore the influence of isoflurane(Iso) on the synthesis of surfactant-related protein(SP-A) of alveolar type II cells(AT II cells) cultured in primary and injured by hydrogen peroxide(H2O2).Methods AT I...Objective To explore the influence of isoflurane(Iso) on the synthesis of surfactant-related protein(SP-A) of alveolar type II cells(AT II cells) cultured in primary and injured by hydrogen peroxide(H2O2).Methods AT II cells were isolated from adult SD rats and used for experiments after 32h in primary culture and randomized into six groups: control group,0.28 mM Iso group,2.8mM Iso group,75 μM H2O2 group,75 μM H2O2 +0.28 mM Iso group and 75 μM H2O2 +2.8 mM Iso group. Each group was continuously incubated for 3 h after administration of Iso or/and H2O2. The intracellular SP-A and the SP-A of cultured medium were measured with an enzyme-linked immunosorbent assay(ELISA).Results Iso significantly decreased SP-A content of cultured medium and the intracellular,and aggravated the decrease of SP-A content induced by H2O2 in a dose-dependent manner.Conclusion Iso itself may decrease SP-A synthesis of AT II cells in vitro,and aggravate the damage of AT II cells especially under peroxidation condition.展开更多
This study investigated the effects of hyperoxia on dynamic changes of thioredoxin-1 （Trx1） and thioredoxin reductase-1 （TrxR1） in alveolar type Ⅱ epithelial cells （AECⅡ） of premature rats. Pregnant Sprague-Da...This study investigated the effects of hyperoxia on dynamic changes of thioredoxin-1 （Trx1） and thioredoxin reductase-1 （TrxR1） in alveolar type Ⅱ epithelial cells （AECⅡ） of premature rats. Pregnant Sprague-Dawley rats were sacrificed on day 19 of gestation. AECⅡ were isolated and purified from the lungs of premature rats. When cultured to 80% confluence, in vitro cells were randomly divided into air group and hyperoxia group. Cells in the hyperoxia group were continuously exposed to 95% O2/5% CO2 and those in the air group to 95% air/5% CO2. After 12, 24 and 48 h, cells in the two groups were harvested to detect their reactive oxygen species （ROS）, apoptosis, TrxR1 activity and the expressions of Trx1 and TrxR1 by corresponding protocols, respectively. The results showed that AECⅡ exposed to hyperoxia generated excessive ROS and the apoptosis percentage in the hyperoxia group was increased significantly at each time points as compared with that in the air group （P0.001）. Moreover, TrxR1 activity was found to be markedly depressed in the hyperoxia group in comparison to that in the air group （P0.001）. RT-PCR showed the expressions of both Trx1 and TrxR1 mRNA were significantly increased in AECⅡ exposed to hyperoxia for 12 and 24 h （P0.01）, respectively. At 48 h, the level of Trx1 mRNA as well as that of TrxR1 mRNA in the hyperoxia group was reduced and showed no significant difference from that in the air group （P0.05）. Western blotting showed the changes of Trx1 protein expressions in the hyperoxia group paralleled those of Trx1 mRNA expressions revealed by RT-PCR. It was concluded that hyperoxia can up-regulate the protective Trx1/TrxR1 expressed by AECⅡ in a certain period, however, also cause dysfunction of the cytoplasmic thioredoxin system by decreasing TrxR1 activity, which may contribute to the progression of oxidative stress and cell apoptosis and finally result in lung injury.展开更多
Smoking during pregnancy is a major source of fetal exposure to numerous harmful agents present in tobacco smoke. Lung development involves complex biochemical processes resulting in dramatic changes which continue ev...Smoking during pregnancy is a major source of fetal exposure to numerous harmful agents present in tobacco smoke. Lung development involves complex biochemical processes resulting in dramatic changes which continue even after birth. In addition to type I cells which form the blood-air barrier, type II alveolar epithelial (AE) cells have important and diverse functions related to immunological protection and stabilization of the alveolus through synthesis and secretion of the pulmonary surfactant. Apoptosis or programmed cells death is an important physiological process during lung embryogenesis and for the proper maintenance of homeostasis. Caspases are proteases that play important roles in regulating apoptosis. Caspase-3 is the key executioner caspase in the cascade of events leading to cell death by apoptosis. We explored the hypothesis that cigarette smoke extract (CSE) induces apoptosis in fetal rat lung type II AE cells by activation of caspase-3. To analyze these factors, isolated fetal rat lung type II AE cells were used. The cells were exposed to different concentrations of CSE (5%, 10% or 15%) (v/v) for 60 min. The results of the present study showed that CSE induced apoptosis in fetal rat lung type II AE cells with a significant increase (p 0.05) in caspase-3 activity and decrease in cell proliferation at CSE concentrations of 10% and 15% (v/v). These observations indicate that cigarette smoke extract induces apoptosis by activation of caspase-3 in fetal rat lung type II AE cells in a dose-dependent manner and may potentially alter the regulated development of the lung and the appearance of the surfactant-producing type II alveolar cells which are critical for the establishment of adequate gas exchange at birth.展开更多
Nanowire-based photovoltaic devices have the advantages over planar devices in light absorption and charge transport and collection.Recently,a new strategy relying on type-Ⅱ band alignment has been proposed to facili...Nanowire-based photovoltaic devices have the advantages over planar devices in light absorption and charge transport and collection.Recently,a new strategy relying on type-Ⅱ band alignment has been proposed to facilitate efficient charge separation in core/shell nanowire solar cells.This paper reviews the type-Ⅱ heterojunction solar cells based on core/shell nanowire arrays,and specifically focuses on the progress of theoretical design and fabrication of type-Ⅱ Zn O/Zn Se core/shell nanowire-based solar cells.A strong photoresponse associated with the type-Ⅱ interfacial transition exhibits a threshold of 1.6 e V,which demonstrates the feasibility and great potential for exploring all-inorganic versions of type-Ⅱ heterojunction solar cells using wide bandgap semiconductors.Future prospects in this area are also outlooked.展开更多
Recent studies have demonstrated that five subtypes （M1-M5） of muscarinic acetylcholine receptor （mAChR） are expressed in the vestibular periphery. However, the exact cellular location of the mAChRs is not clear. ...Recent studies have demonstrated that five subtypes （M1-M5） of muscarinic acetylcholine receptor （mAChR） are expressed in the vestibular periphery. However, the exact cellular location of the mAChRs is not clear. In this study, we investigated whether there is the expression of M1-M5 muscarinic receptor mRNA in isolated type Ⅱ vestibular hair cells of guinea pig by using single-cell RT-PCR. In vestibular end-organ, cDNA of the expected size was obtained by RT-PCR. Moreover, mRNA was identified by RT-PCR from individually isolated type Ⅱ vestibular hair cells （single-cell RT-PCR）. Sequence analysis confirmed that the products were M1-M5 mAChR. These results dem-onstrated that M1-M5 mAChR was expressed in the typeⅡvestibular hair cells of the guinea pig, which lends further support for the role of M1-M5 mAChR as a mediator of efferent cholinergic signalling pathway in vestibular hair cells.展开更多
Pulmonary fibrosis(PF)is a lethal lung disease that predominantly affects older adults;however,whether and how aging triggers fibrosis remains unclear.To pinpoint the predominant initiating factors of PF,we first anal...Pulmonary fibrosis(PF)is a lethal lung disease that predominantly affects older adults;however,whether and how aging triggers fibrosis remains unclear.To pinpoint the predominant initiating factors of PF,we first analyzed single-cell RNA sequencing(scRNA-seq)data from the lung tissues of 45 normal donors and 51 PF patients and found that aging might serve as the primary catalyst for PF development.To further investigate the influence of aging on PF formation,we conducted a comprehensive and thorough study employing a natural aging mouse model.We found that dynamic alterations in the quantity and types of collagen fibers during aging-induced PF progression,especially in collagenous(Col)I,emerged as the predominant driver of PF.We then investigated the regulation of Col I synthesis during aging using primary alveolar type 2(AT2)cells and A549 cells line through conditioned media and Transwell cocul-ture,and found that secretions—particularly plasminogen activator inhibitor(PAI)-1—from aged AT2 cells promoted fibrosis and enhanced collagen type I alpha 1(Col1al)production via the transforming growth factor(TGF)-b/small mother against decapentaplegic(Smad)2/3 pathway.Furthermore,scRNA-seq and a histological analysis of human lung tissue demonstrated a significant upregulation of SERPINE1(the gene encoding PAI-1)and PAI-1 expression in both aging lung tissue and AT2 cells,which was consistent with our findings from animal experiments,providing additional evidence for the pivotal role of PAI-1 during aging and the development of PF.Our research demonstrates that PAI-1,a crucial factor secreted by aging AT2 cells,exerts a pivotal role in promoting the synthesis of Col1a1 in fibroblasts,subsequently leading to Col I deposition,and in driving the progression of PF by mediating the TGF-b/Smad2/3 pathway.Our find-ings offer critical evidence for the involvement of epithelial dysfunction in age-related PF and provides potential novel therapeutic targets for clinical intervention.展开更多
基金supported by the National Natural Sciences Foundation of China(31730051 and 31601164)the National Key Research and Development Program of China(2018YFA0800900)+1 种基金Natural Science Foundation of Shandong Province,China(ZR2019PH076)the Open Project of Forensic Medicine Key Laboratory of Shanxi Province,China(SFM2019001)。
文摘Pulmonary surfactant is a lipid-protein complex secreted by alveolar typeⅡepithelial cells and is essential for the maintenance of the delicate structure of mammalian alveoli to promote efficient gas exchange across the air-liquid barrier.The Golgi apparatus plays an important role in pulmonary surfactant modification and secretory trafficking.However,the physiological function of the Golgi apparatus in the transport of pulmonary surfactants is unclear.In the present study,deletion of GM130,which encodes for a matrix protein of the cis-Golgi cisternae,was shown to induce the disruption of the Golgi structure leading to impaired secretion of lung surfactant proteins and lipids.Specifically,the results of in vitro and in vivo analysis indicated that the loss of GM130 resulted in trapping of Sftpa in the endoplasmic reticulum,Sftpb and Sftpc accumulation in the Golgi apparatus,and an increase in the compensatory secretion of Sftpd.Moreover,global and epithelial-specific GM130 knockout in mice resulted in an enlargement of alveolar airspace and an increase in alveolar epithelial autophagy;however,surfactant repletion partially rescued the enlarged airspace defects in GM130-deficient mice.Therefore,our results demonstrate that GM130 and the mammalian Golgi apparatus play a critical role in the control of surfactant protein secretion in pulmonary epithelial cells.
文摘Summary: The pathogenesis of hyperoxia lung injury and the mechanism of amygdalin on type 2 alveolar epithelial cells (AEC2) isolated from premature rat lungs in vitro were investigated. AEC2 were obtained by primary culture from 20-days fetal rat lung and hyperoxia-exposed cell model was established. Cell proliferating viability was examined by MTT assay after treatment of amygdalin at various concentrations. DNA content and the proliferating cell nuclear antigen (PCNA) protein expression of AEC2 were measured by using flow cytometry and immunocytochemistry respectively after 24 h of hyperoxia exposure or amygdalin treatment. The results showed that hyperoxia inhibited the proliferation and decreased PCNA protein expression in AEC2 of premature rat in vitro. Amygdalin at the concentration range of 50-200 μmol/L stimulated the proliferation of AEC2 in a dose-dependent manner, however, 400 μmol/L amygdalin inhibited the proliferation of AEC2. Amygdalin at the concentration of 200 μmol/L played its best role in facilitating proliferation of AEC2s in vitro and could partially ameliorated the changes of proliferation in hyperoxia exposed AEC2 of premature rat. It has been suggested that hyperoxia inhibited the proliferation of AEC2s of premature rat, which may contribute to hyperoxia lung injury. Amygdalin may play partial protective role in hyperoxia-induced lung injury.
基金the National Natural Sciences Foundation of China (No. 30500224 and No. 30400193).
文摘To establish a better method of primary culture for alveolar epithelial type Ⅱ cells （AEC Ⅱ ） and to study its bionomics, alveolar epithelial type Ⅱ cells were isolated by digestion with trypsin and collagenase, which were then purified by plated into culture flask coated with rat immunoglobulin （i The purified AEC Ⅱ were identified by alkaline phosphatase staining, electron mi- croscopy, immunocytochemical staining of pulmonary surfactant protein A （SPA）. The SPA expression and transfection characteristics were compared with those of A549 cell line. The results showed that AEC Ⅱ could be isolated by digestion with trysin and collagenase and purified by adhesive purification by using IgG, with a yield of about 2-3 × 10^7, and a purity of about 75%-84 %. Cells could be quickly identified with AKP staining. AEC Ⅱ were different from A549 cell line in terms of SPA expression and transfection characteristics. It is concluded that adhesive purification with IgG can improve the purity of AEC Ⅱ, and AKP staining is simple in cell identification. AEC Ⅱ can not be completely replaced by A549 cells in some studies because the differences between them, such as SPA expression.
文摘Objective:To investigate the effects of mechanical stretching and lipopolysaccharide(LPS) on the early apoptosis and IL-8 production of alveolar epithelial type II cells A549.Methods:The experimental matrix consisted of three integrated studies.In the first study,A549 cells were subjected to different stretching strain frequency and duration time to see the effects on the early apoptosis.In the second study,A549 cells were subjected to mechanical stretch(13%4 h, 0.3 Hz) and LPS(1 or 100 ng/mL) to see whether mechanical strain and LPS also have an addictive effect on the early apoptosis.In the third study to investigate whether this addictive effect could be induced by LPS and mechanical stretch on IL-8 production,A549 cells were subjected to LPS(100 ng/mL) and mechanical strain(13%.0.3 Hz,4 h).Real time PCR and enzyme linked immunosorbent assay were used to measure mRN A and protein level of IL-8.The early apoptosis was detected by flow cytometry.Results:Mechanical stretch induced the early apoptosis in a force and frequency and time-dependent manner.In the presence of LPS,mechanical stretch enhanced LPS-induced early apoptosis,especially in 100 ng/mL IPS group compared with 1 ng/ mL LPS and the control group.Mechanical stretch increased IL-8 production and enhanced LPS-induced IL-8 screation both in mRNA and protein levels.Conclusions:Mechanical stretch can induce the early apoptosis and IL-8 secretion.Mechanical stretch and LPS have an addictive effect on the early apoptosis and IL-8 production in alveolar type 2 cells,which is one of the mechanisms of ventilator-induced lung injury.
文摘Objective To explore the influence of isoflurane(Iso) on the synthesis of surfactant-related protein(SP-A) of alveolar type II cells(AT II cells) cultured in primary and injured by hydrogen peroxide(H2O2).Methods AT II cells were isolated from adult SD rats and used for experiments after 32h in primary culture and randomized into six groups: control group,0.28 mM Iso group,2.8mM Iso group,75 μM H2O2 group,75 μM H2O2 +0.28 mM Iso group and 75 μM H2O2 +2.8 mM Iso group. Each group was continuously incubated for 3 h after administration of Iso or/and H2O2. The intracellular SP-A and the SP-A of cultured medium were measured with an enzyme-linked immunosorbent assay(ELISA).Results Iso significantly decreased SP-A content of cultured medium and the intracellular,and aggravated the decrease of SP-A content induced by H2O2 in a dose-dependent manner.Conclusion Iso itself may decrease SP-A synthesis of AT II cells in vitro,and aggravate the damage of AT II cells especially under peroxidation condition.
基金supported by a grant from the National Natural Sciences Foundation of China (No. 30770944)
文摘This study investigated the effects of hyperoxia on dynamic changes of thioredoxin-1 （Trx1） and thioredoxin reductase-1 （TrxR1） in alveolar type Ⅱ epithelial cells （AECⅡ） of premature rats. Pregnant Sprague-Dawley rats were sacrificed on day 19 of gestation. AECⅡ were isolated and purified from the lungs of premature rats. When cultured to 80% confluence, in vitro cells were randomly divided into air group and hyperoxia group. Cells in the hyperoxia group were continuously exposed to 95% O2/5% CO2 and those in the air group to 95% air/5% CO2. After 12, 24 and 48 h, cells in the two groups were harvested to detect their reactive oxygen species （ROS）, apoptosis, TrxR1 activity and the expressions of Trx1 and TrxR1 by corresponding protocols, respectively. The results showed that AECⅡ exposed to hyperoxia generated excessive ROS and the apoptosis percentage in the hyperoxia group was increased significantly at each time points as compared with that in the air group （P0.001）. Moreover, TrxR1 activity was found to be markedly depressed in the hyperoxia group in comparison to that in the air group （P0.001）. RT-PCR showed the expressions of both Trx1 and TrxR1 mRNA were significantly increased in AECⅡ exposed to hyperoxia for 12 and 24 h （P0.01）, respectively. At 48 h, the level of Trx1 mRNA as well as that of TrxR1 mRNA in the hyperoxia group was reduced and showed no significant difference from that in the air group （P0.05）. Western blotting showed the changes of Trx1 protein expressions in the hyperoxia group paralleled those of Trx1 mRNA expressions revealed by RT-PCR. It was concluded that hyperoxia can up-regulate the protective Trx1/TrxR1 expressed by AECⅡ in a certain period, however, also cause dysfunction of the cytoplasmic thioredoxin system by decreasing TrxR1 activity, which may contribute to the progression of oxidative stress and cell apoptosis and finally result in lung injury.
文摘Smoking during pregnancy is a major source of fetal exposure to numerous harmful agents present in tobacco smoke. Lung development involves complex biochemical processes resulting in dramatic changes which continue even after birth. In addition to type I cells which form the blood-air barrier, type II alveolar epithelial (AE) cells have important and diverse functions related to immunological protection and stabilization of the alveolus through synthesis and secretion of the pulmonary surfactant. Apoptosis or programmed cells death is an important physiological process during lung embryogenesis and for the proper maintenance of homeostasis. Caspases are proteases that play important roles in regulating apoptosis. Caspase-3 is the key executioner caspase in the cascade of events leading to cell death by apoptosis. We explored the hypothesis that cigarette smoke extract (CSE) induces apoptosis in fetal rat lung type II AE cells by activation of caspase-3. To analyze these factors, isolated fetal rat lung type II AE cells were used. The cells were exposed to different concentrations of CSE (5%, 10% or 15%) (v/v) for 60 min. The results of the present study showed that CSE induced apoptosis in fetal rat lung type II AE cells with a significant increase (p 0.05) in caspase-3 activity and decrease in cell proliferation at CSE concentrations of 10% and 15% (v/v). These observations indicate that cigarette smoke extract induces apoptosis by activation of caspase-3 in fetal rat lung type II AE cells in a dose-dependent manner and may potentially alter the regulated development of the lung and the appearance of the surfactant-producing type II alveolar cells which are critical for the establishment of adequate gas exchange at birth.
基金supported by "973" Program (No.2012CB619301 and 2011CB925600)the National Natural Science Foundations of China (No.61227009,61106008,61106118,90921002,and 60827004)+1 种基金the Natural Science Foundations of Fujian Provincethe fundamental research funds for the central universities (No.2011121042 and 2011121026)
文摘Nanowire-based photovoltaic devices have the advantages over planar devices in light absorption and charge transport and collection.Recently,a new strategy relying on type-Ⅱ band alignment has been proposed to facilitate efficient charge separation in core/shell nanowire solar cells.This paper reviews the type-Ⅱ heterojunction solar cells based on core/shell nanowire arrays,and specifically focuses on the progress of theoretical design and fabrication of type-Ⅱ Zn O/Zn Se core/shell nanowire-based solar cells.A strong photoresponse associated with the type-Ⅱ interfacial transition exhibits a threshold of 1.6 e V,which demonstrates the feasibility and great potential for exploring all-inorganic versions of type-Ⅱ heterojunction solar cells using wide bandgap semiconductors.Future prospects in this area are also outlooked.
基金supported by grants from the Key Project of National Natural Science Foundation of China (No. 30730094)the National Science & Technology Pillar Program during the Eleventh Five-year Plan Period (No. 2007BAI18B13)+1 种基金the National Natural Science Foundation of China (No. 30872865)the National High Technology Research and Development Program of China (Program 863) (No. 2008AA02Z428)
文摘Recent studies have demonstrated that five subtypes （M1-M5） of muscarinic acetylcholine receptor （mAChR） are expressed in the vestibular periphery. However, the exact cellular location of the mAChRs is not clear. In this study, we investigated whether there is the expression of M1-M5 muscarinic receptor mRNA in isolated type Ⅱ vestibular hair cells of guinea pig by using single-cell RT-PCR. In vestibular end-organ, cDNA of the expected size was obtained by RT-PCR. Moreover, mRNA was identified by RT-PCR from individually isolated type Ⅱ vestibular hair cells （single-cell RT-PCR）. Sequence analysis confirmed that the products were M1-M5 mAChR. These results dem-onstrated that M1-M5 mAChR was expressed in the typeⅡvestibular hair cells of the guinea pig, which lends further support for the role of M1-M5 mAChR as a mediator of efferent cholinergic signalling pathway in vestibular hair cells.
基金supported by the Young Elite Scientist Sponsorship Program by CAST(2022QNRC001)the 111 project of the Education Ministry of China(B18053).
文摘Pulmonary fibrosis(PF)is a lethal lung disease that predominantly affects older adults;however,whether and how aging triggers fibrosis remains unclear.To pinpoint the predominant initiating factors of PF,we first analyzed single-cell RNA sequencing(scRNA-seq)data from the lung tissues of 45 normal donors and 51 PF patients and found that aging might serve as the primary catalyst for PF development.To further investigate the influence of aging on PF formation,we conducted a comprehensive and thorough study employing a natural aging mouse model.We found that dynamic alterations in the quantity and types of collagen fibers during aging-induced PF progression,especially in collagenous(Col)I,emerged as the predominant driver of PF.We then investigated the regulation of Col I synthesis during aging using primary alveolar type 2(AT2)cells and A549 cells line through conditioned media and Transwell cocul-ture,and found that secretions—particularly plasminogen activator inhibitor(PAI)-1—from aged AT2 cells promoted fibrosis and enhanced collagen type I alpha 1(Col1al)production via the transforming growth factor(TGF)-b/small mother against decapentaplegic(Smad)2/3 pathway.Furthermore,scRNA-seq and a histological analysis of human lung tissue demonstrated a significant upregulation of SERPINE1(the gene encoding PAI-1)and PAI-1 expression in both aging lung tissue and AT2 cells,which was consistent with our findings from animal experiments,providing additional evidence for the pivotal role of PAI-1 during aging and the development of PF.Our research demonstrates that PAI-1,a crucial factor secreted by aging AT2 cells,exerts a pivotal role in promoting the synthesis of Col1a1 in fibroblasts,subsequently leading to Col I deposition,and in driving the progression of PF by mediating the TGF-b/Smad2/3 pathway.Our find-ings offer critical evidence for the involvement of epithelial dysfunction in age-related PF and provides potential novel therapeutic targets for clinical intervention.
