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机构地区:[1]浙江大学医学院附属第二医院眼科中心,杭州310009
出 处:《眼科研究》2007年第11期809-813,共5页Chinese Ophthalmic Research
基 金:卫生部科学研究基金(491020-W10555);浙江省科学技术厅研究基金(491020-J30526)资助
摘 要:目的探讨转化生长因子β2(TGF-β2)对晶状体上皮细胞(LECs)增生和上皮间质转分化的影响。方法体外培养的人LECs株HLE-B3,加入不同质量浓度的TGF-β2进行处理,分别采用MTT法测定其对细胞增生的影响;采用PI细胞周期染色分析检测细胞周期的改变;应用Western blot及免疫荧光分别检测connexin43、fibronectin及integrinβ1等转分化相关蛋白表达的变化。结果经TGF-β2处理后的细胞增生受到抑制,呈TGF-β2质量浓度和时间依赖性;细胞周期中S期细胞的比例明显降低;connexin43表达随TGF-β2处理时间的增加而逐渐降低,fibronectin及integrinβ1的表达则随TGF-β2处理时间的增加而逐渐上升。结论TGF-β2抑制了LECs的增生,显著下调LECs connexin43的表达,促进了细胞外基质的过度沉积,对后发性白内障的防治具有一定的应用前景。Objective Research showed that transforming growth factor-β(TGF-β) promotes or suppresses the proliferation and epithelial mesenchymal transition and therefore participates in muhiful biological procedure. This study aimed to investigate the effect of TGF-β2 on proliferation and epithelial mesenchymal transition in human lens epithelial cells( HLECs). Methods HLE-β3 cell strain was cultured and passaged. The 10 th generation of HLECs were treated with different concentrations of TGF-β2 for indicated times. The cell survival rate was assayed by MTT. The cell cycle distribution was assayed by flow cytometry(FCM). The changes of the expression of eonnexin 43, fibroneetin and integrin β1 were examined by Western blot and immunofluorescence. Results The proliferation of cultured HLECs was suppressed significantly after treatment of TGF-β2 in a dose-and time-dependent manner with the strongest effect in 100 pg/mL TGF-β2 at 48 hours group. The percentage of S phage of cells was significantly decreased in 100 pg/mL TGF-β2 for 48 hours group (9.0% ± 2.6% ) in comparison with control group (24. 3% ± 2.1% )( P = 0. 00). The expression of connexin 43 was decreased after treatment of TGF-β2 ;while the expression of fibronectin and integrin β1 was increased. Conclusion TGF-β2 inhibits the proliferation and induces the epithelial mesenchymal transition of HLECs. The mechanism of proliferation and epithelial mesenchymal transition of HLECs may be involved in the formation process of posterior capsular opacification.
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