自噬信号因子P70S6K参与Cox7a2调控睾酮生成机制研究

P70S6K is involved in the inhibition of testosterone production in TM3 mouse Leydig cells overexpressing Cox7a2

目的:研究Cox7a2对TM3 Leydig细胞睾酮生成的影响以及涉及其中的自噬调控信号的作用。方法:构建Cox7a2荧光表达载体,转染TM3 Leydig细胞。ELISA测定睾酮水平,Western印迹检测Cox7a2对睾酮合成快速调节蛋白StAR表达和自噬调控因子P70S6K磷酸化水平的影响。结果:在TM3 Leydig细胞中,LH刺激能增加促进StAR蛋白表达,增加睾酮合成水平。Cox7a2在TM3小鼠睾丸Leydig细胞中抑制P70S6K磷酸化水平,降低StAR蛋白的表达,进而抑制LH诱导的睾酮合成。结论:Cox7a2通过抑制快速调节蛋白StAR的表达减少LH诱导的睾酮分泌,这至少和Cox7a2抑制自噬调控因子P70S6K有关。

Objective： To investigate the effects of Cox7a2 on the LH-induced testosterone production and the involved autoph- agy regulating signals in TM3 mouse Leydig cells. Methods： The Cox7a2-pEYFP-N1 fluorescent protein vector was constructed and transfected into TM3 mouse Leydig ceils. The level of testosterone was determined by ELISA, and the effects of Cox7a2 on the expression of the steroidogenic acute regulatory protein （STAR） and the phosphorylation of the autophagy regulatory factor P70S6K were detec- ted by Western blot. Results： LH stimulation increased the StAR protein expression and testosterone production, while Cox7a2 de- creased P70S6K phosphory｜ation, reduced StAR expression and consequently inhibited LH-induced testosterone biosynthesis in the TM3 Leydig ceils. Conclusion： Cox7a2 inhibits testosterone production by decreasing the StAR protein expression, which might be at least in part related with the activation of autopbagy in TM3 mouse Leydig cells.