尾加压素Ⅱ体外促进晶状体上皮细胞增殖的细胞信号转导机制

Mechanism on signal transduction of proliferation induced by urotensin Ⅱ in lens epithelial cell

目的:探讨尾加压素Ⅱ(urotensinⅡ,U-Ⅱ)促进晶状体上皮细胞(lens epithelial cell,LEC)增殖的细胞信号转导机制。方法:采用U-Ⅱ与体外培养的LEC共同孵育,并用4种细胞信号转导阻断剂H7,PD98059,W7,尼卡地平(nicardipine)分别作用于LEC,再用3H胸腺嘧啶(3H-TdR)掺入法检测LEC增殖的情况。结果:U-Ⅱ组LEC的3H掺入放射活性显著高于对照组(P<0.01),4种信号转导阻断剂组的放射活性与U-Ⅱ组比较均有不同程度的降低(P<0.01,P<0.01)。PD98059和H7的阻断作用强于nicardipine和W7(F=13.251,P<0.01)。结论:尾加压素Ⅱ促进LEC增殖是通过细胞信号转导的机制,该作用可被信号转导阻断剂所阻断。

AIM：To study the mechanism on signal transduction of proliferation induced by urotensin-Ⅱ （U-Ⅱ） in lens epithelial cell（LEC）. METHODS： U-Ⅱ were incubated with cultured LEC. Meanwhile four blockers of signal transduction, H7, PD98059, W7 and nicardipine, were incubated with LEC separately. Then the proliferations of LEC were detected via ^3H-TdR incorporation. RESULTS：The radioactivity of ^3H-TdR in U-Ⅱ group was higher than that in control group （ P 〈 0. 01 ）. The radioactivities of 3H-TdR in groups of four blockers decreased in varying degrees compared with U-Ⅱ group （ P〈 0.01, P〈 0.01 ）. The blocking effects of PD98059 and H7 were higher than that of nicardipine and W7 （ F = 13. 251, P 〈 0.01）. CONCLUSION ： U- Ⅱ induced LEC proliferation by means of signal trasduction which can be blocked by four signal transduction blockers. The result provides a new thinking for prevention and treatment of after cataract.