Jing Jun, Chen Li, Fu Hai-Yan, Fan Kai, Yao Qi, Ge Yi-Feng, Lu Jin-Chun, Yao Bing
Center of Reproductive Medicine, Nanjing Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China.
Sci Rep. 2015 Mar 24;5:9437. doi: 10.1038/srep09437.
This study investigated the effect of annexin V on the proliferation of primary rat Leydig cells and the potential mechanism. Our results showed that annexin V promoted rat Leydig cell proliferation and cell cycle progression in a dose- and time-dependent manner. Increased level of annexin V also enhanced Ect2 protein expression. However, siRNA knockdown of Ect2 attenuated annexin V-induced proliferation of rat Leydig cells. Taken together, these data suggest that increased level of annexin V induced rat Leydig cell proliferation and cell cycle progression via Ect2. Since RhoA activity was increased following Ect2 activation, we further investigated whether Ect2 was involved in annexin V-induced proliferation via the RhoA/ROCK pathway, and the results showed that annexin V increased RhoA activity too, and this effect was abolished by the knockdown of Ect2. Moreover, inhibition of the RhoA/ROCK pathway by a ROCK inhibitor, Y27632, also attenuated annexin V-induced proliferation and cell cycle progression. We thus conclude that Ect2 is involved in annexin V-induced rat Leydig cell proliferation through the RhoA/ROCK pathway.
本研究调查了膜联蛋白V对原代大鼠睾丸间质细胞增殖的影响及其潜在机制。我们的结果表明，膜联蛋白V以剂量和时间依赖性方式促进大鼠睾丸间质细胞增殖和细胞周期进程。膜联蛋白V水平的升高还增强了Ect2蛋白的表达。然而，Ect2的小干扰RNA敲低减弱了膜联蛋白V诱导的大鼠睾丸间质细胞增殖。综上所述，这些数据表明膜联蛋白V水平的升高通过Ect2诱导大鼠睾丸间质细胞增殖和细胞周期进程。由于Ect2激活后RhoA活性增加，我们进一步研究Ect2是否通过RhoA/ROCK途径参与膜联蛋白V诱导的增殖，结果表明膜联蛋白V也增加了RhoA活性，而这种作用在Ect2敲低后被消除。此外，ROCK抑制剂Y27632对RhoA/ROCK途径的抑制也减弱了膜联蛋白V诱导的增殖和细胞周期进程。因此，我们得出结论，Ect2通过RhoA/ROCK途径参与膜联蛋白V诱导的大鼠睾丸间质细胞增殖。
