Amyotrophic lateral syndrome(ALS)is a progressive degenerative disorder characterized by motor neuron death and axon degeneration.Mitochondrial dysfunction plays a key role in the pathogenesis of ALS,the mechanism of ...Amyotrophic lateral syndrome(ALS)is a progressive degenerative disorder characterized by motor neuron death and axon degeneration.Mitochondrial dysfunction plays a key role in the pathogenesis of ALS,the mechanism of which remains poorly understood.The B-cell lymphoma-2(Bcl-2)family of proteins that control and mediate mitochondrial function and apoptosis,including the pro-apoptotic members Bcl2-Associated X(Bax),are involved in ALS development.The death receptor 6(DR6)regulates motor neuron death in ALS,and DR6 antibodies can prevent axon degeneration and motor neuron damage by blocking DR6.Previous studies demonstrated that PSAP localized to mitochondria and was required for DR6-induced apoptosis.In this study,SOD1^(G93A) was transfected into the motor neuron cell line NSC-34 to serve as an ALS cell model in vitro.The data assessed the role of PSAP in SOD1^(G93A)induced apoptosis and demonstrated that the overexpression of SOD1^(G93A),but not wtSOD1,induced PARP cleavage,caspase-3 activation,cytochrome c release,and Bax translocation.PSAP,Bax,and Bak were necessary for SOD1^(G93A)induced apoptosis,as silencing PSAP inhibited SOD1^(G93A)-mediated cell death that was dependent on Bax-Bak interaction.展开更多
Objective To investigate the prosaposin （PSAP） expression in polycystic ovaries. Methods The expression of PSAP was examined using immunohistochemistry, quantitative RT-PCR and Western blotting in a rat model with l...Objective To investigate the prosaposin （PSAP） expression in polycystic ovaries. Methods The expression of PSAP was examined using immunohistochemistry, quantitative RT-PCR and Western blotting in a rat model with letrozole-induced polycystic ovary syndrom （PCOS）. Results Letrozole-induced PCOS rat models were similar to those in human PCOS in endocrine disturbances, metabolic characteristics and morphology features. And in these models both mRNA and protein levels of PSAP were significantly increased. Conclusion PSAP was overexpressed in the letrozole-induced PCOS rat model and might play an important role in the oceurance and development of PCOS.展开更多
基金supported by grants from the National Natural Science Foundation of China[Grant No.81701076,Linlin Zeng]the Science and Technology Department of Jilin Province[Grant No.20190701037GH,Fuqiang Zhang+2 种基金Grant No.20190701036GH,Linlin Zengand Grant No.20200201386JC,Guodong Li]the Education Department of Jilin Province[Grant No.JJKH20200948KJ,Linlin Zeng]。
文摘Amyotrophic lateral syndrome(ALS)is a progressive degenerative disorder characterized by motor neuron death and axon degeneration.Mitochondrial dysfunction plays a key role in the pathogenesis of ALS,the mechanism of which remains poorly understood.The B-cell lymphoma-2(Bcl-2)family of proteins that control and mediate mitochondrial function and apoptosis,including the pro-apoptotic members Bcl2-Associated X(Bax),are involved in ALS development.The death receptor 6(DR6)regulates motor neuron death in ALS,and DR6 antibodies can prevent axon degeneration and motor neuron damage by blocking DR6.Previous studies demonstrated that PSAP localized to mitochondria and was required for DR6-induced apoptosis.In this study,SOD1^(G93A) was transfected into the motor neuron cell line NSC-34 to serve as an ALS cell model in vitro.The data assessed the role of PSAP in SOD1^(G93A)induced apoptosis and demonstrated that the overexpression of SOD1^(G93A),but not wtSOD1,induced PARP cleavage,caspase-3 activation,cytochrome c release,and Bax translocation.PSAP,Bax,and Bak were necessary for SOD1^(G93A)induced apoptosis,as silencing PSAP inhibited SOD1^(G93A)-mediated cell death that was dependent on Bax-Bak interaction.
基金a Colleges and Universities Scientific Program supported by Education Department of Liaoning Province (LT2010106)
文摘Objective To investigate the prosaposin （PSAP） expression in polycystic ovaries. Methods The expression of PSAP was examined using immunohistochemistry, quantitative RT-PCR and Western blotting in a rat model with letrozole-induced polycystic ovary syndrom （PCOS）. Results Letrozole-induced PCOS rat models were similar to those in human PCOS in endocrine disturbances, metabolic characteristics and morphology features. And in these models both mRNA and protein levels of PSAP were significantly increased. Conclusion PSAP was overexpressed in the letrozole-induced PCOS rat model and might play an important role in the oceurance and development of PCOS.
