%0 Journal Article
%T TGF-β2诱导晶状体上皮细胞凋亡的机制<br>Molecular mechanisms underlying TGF-β2 induced apoptosis of human lens epithelial cells
%A 景瑞花
%A 齐甜甜
%A 张 明
%A 岳嘉琦
%A 王光妍
%A 裴 澄
%A 马 波
%J 西安交通大学学报(医学版)
%D 2019
%R 10.7652/jdyxb201905012
%X 摘要：目的 探讨晶状体后囊膜混浊(posterior capsular opacification, PCO)过程中转化生长因子-β2(transforming growth factor β2, TGF-β2)诱导晶状体上皮细胞(human lens epithelial cell, HLEC)凋亡的机制。方法 用不同浓度TGF-β2(0、0.1、1、10μg/L)处理HLEC后，Western blot检测TGF-β2诱导的线粒体途径依赖的细胞凋亡相关蛋白表达；流式细胞仪检测5μg/L TGF-β2诱导细胞凋亡的具体形式，以及5μg/L TGF-β2处理细胞36h对细胞周期的影响。结果 TGF-β2可明显增加Caspase3的表达(P<0.001)，促凋亡蛋白Bax与抑凋亡蛋白Bcl-2的表达比例失调(P<？？0.001？？)并呈浓度依赖性，激活内源性线粒体途径的Bax/Bcl-2-caspase3通路的凋亡。5μg/L的TGF-β2可以诱导HLEC发生凋亡(P<0.05)，处理细胞36h后可导致G1/S周期阻滞。结论 PCO过程中伴随TGF-β2诱导的线粒体途经的细胞凋亡，可能参与了PCO的形成过程，将为PCO发病机理及药物开发提供新思路。<br>ABSTRACT: Objective To investigate the effects of transforming growth factor-beta 2 (TGF-β2) on the apoptosis of human lens epithelial cells (HLECs) in posterior capsular opacification (PCO). Methods Different concentration (0, 0.1, 1, and 10μg/L) of TGF-β2 was added into HLECs to induce cell apoptosis and Western blot was applied to analyze the expression levels of endogenous mitochondrial pathway-dependent apoptosis-associated proteins. Flow cytometry was used to measure the cell apoptosis and cell cycle arrest induced by 5μg/L of TGF-β2. Results TGF-β2 was sufficient to significantly increase the expression of apoptosis-associated proteins such as Caspase3 (P<0.001) and expression imbalance of Bcl-2/Bax (P<0.001) in the concentration-dependent manner, indicating the activation of endogenous mitochondrial apoptosis pathway. Stimulation of 5μg/L of TGF-β2 was enough to induce cell apoptosis (P<0.05). After induction for 36 h, obvious G1/S cell cycle arrest was observed. Conclusion TGF-β2 was involved in the mitochondrial apoptosis pathway and PCO. Our findings might provide new insights into the pathogenesis and new drug exploitation for PCO
%K 后发性白内障
%K 转化生长因子-β2
%K 细胞凋亡<br>posterior capsular opacification
%K TGF-β2
%K cell apoptosis
%U http://yxxb.xjtu.edu.cn//oa/darticle.aspx?type=view&id=201905012