| 1 | EMC10 governs male fertility via maintaining sperm ion balance显示文摘Infertility is a severe public health problem worldwide that prevails up to 15% in reproductive-age couples,and male infertility accounts for half of total infertility.Studies on genetically modified animal models have identifed lots of genes involved in the pathogenesis of male infertility.The underlying causes,however,remain largely unclear.In this study,we provide evidence that EMCIO,one subunit of endoplasmic reticulum (ER)membrane protein complex (EMC),is required for male fertility.EMC10 is significantly decreased in spermatozoa from patients with asthenozoospermia and positively associated with human sperm motility. Male mice lacking Emc10 gene are completely sterile.Emc10-null spermatozoa exhibit multiple defects including abnormal morphology,decreased motility,impaired capacitation,and impotency of acrosome reaction,thereby which are incapable of fertilizing intact or ZP-free oocytes.However,intracytoplasmic sperm injection could rescue this defect caused by EMC10 deletion. Mechanistically,EMC10 deficiency leads to inactivation of Na/K-ATPase,in turn giving rise to an increased level of intraceltutar Na^+ in spermatozoa,which contributes to decreased sperm motility and abnormal morphology.Other mechanistic investigations demonstrate that the absence of EMC10 results in a reduction of HCO3^- entry and subsequent decreases of both cAMP-dependent protein kinase A substrate phosphorylation and protein tyrosine phosphorytation.These data demonstrate that EMC10 is indispensable to mate fertility via maintaining sperm ion balance of Na^+ and HCO3^-,and also suggest that EMC10 is a promising biomarker for male fertility and a potential pharmaceutical target to treat male infertility. | Yuchuan Zhou Fei Wu Man Zhang Zuquan Xiong Qianqian Yin Yanfei Ru Huijuan Shi Jinsong Li Shanhua Mao Yanliang Li Xinyi Cao Renming Hu Chong Wee Liew Qiang Ding Xuanchun Wang Yonglian Zhang | 2018 | Journal of Molecular Cell Biology2018，10，6： | 2 |
| 3 | Bisphenol A accelerates capacitation-associated protein tyrosine phosphorylation of rat sperm by activating protein kinase A显示文摘Bisphenol A (BPA ) 是合成雌激素模仿化学药品。影响许多繁殖端点被显示了。然而,成熟精子和它的行动的机制上的 BPA 的效果还不是清楚的。这里,我们的在里面 vitro 研究显示 BPA 能加速精子在 time-dependentmanners 和 dose-dependentmanners 的联系 capacitation 的蛋白质酷氨酸 phosphorylation。在 vivo,暴露于 BPA 的高剂量的成年雄的老鼠能导致精子活动的重要增加。进一步的 investigationdemonstrated 就算精子是缺乏 BSA, HCO 3-, 和 Ca 2+ 的 incubatedin 媒介,那 BPA 能加速联系 capacitation 的蛋白质酷氨酸 phosphorylation。然而, BPA 刺激的这个行动能被 H89 堵住,蛋白质 kinase A (PKA ) 的高度选择的 blocker,由 KH7 的 butnot, adenylyl cyclase 的一个特定的禁止者。这些数据建议 BPA 可以激活 PKA 影响精子 functionsand 男性富饶。 | Xiaofeng Wan Yanfei Ru Chen Chu Zimei Ni Yuchuan Zhou Shoulin Wang Zuomin Zhou Yonglian Zhang | 2016 | Acta Biochimica et Biophysica Sinica2016，48，6： | 0 |
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