CAJ | 학술논문

目的观察雌激素受体α(ERα)在17β-雌二醇(E2)促进小鼠前列腺平滑肌细胞(PSMC)增殖中的作用,探讨E2对PSMC的作用机制.方法构建pGSadeno-ERα腺病毒载体,体外转染原代培养的小鼠前列腺平滑肌细胞(PSMC),将实验细胞分组:实验组;ERα基因下调组,细胞转染ERα干扰序列腺病毒;阴性对照组,细胞转染无义序列腺病毒;正常对照组,正常的小鼠PSMC.各组分别加入1×10-8mol/L E2,72 h后流式细胞仪检测细胞增殖,Western blot检测细胞内Cyclin D1基因表达.结果 E2作用细胞72 h后,实验组细胞G0/G1期的比率(71.76±1.78)%显著高于阴性对照组(51.73±1.86)%和正常对照组(47.90±0.79)%,差异有统计学意义(P＜0.05);相对应的PI值:实验组(28.24±1.78)显著低于阴性对照组(47.27±1.86)和正常对照组(52.10±0.79)比较,差异有统计学意义(P＜0.05);实验组细胞内Cyclin D1基因表达水平显著低于对照组.结论雌激素在对前列腺平滑肌细胞的生物学效应中,通过雌激素受体α的介导调控了细胞周期素Cyclin D1的表达,从而促进细胞的增殖.
목적 관찰자격소수체α(ERα)재17β-자이순(E2)촉진소서전렬선평활기세포(PSMC)증식중적작용,탐토E2대PSMC적작용궤제.방법 구건pGSadeno-ERα선병독재체,체외전염원대배양적소서전렬선평활기세포(PSMC),장실험세포분조:실험조;ERα기인하조조,세포전염ERα간우서렬선병독;음성대조조,세포전염무의서렬선병독;정상대조조,정상적소서PSMC.각조분별가입1×10-8mol/L E2,72 h후류식세포의검측세포증식,Western blot검측세포내Cyclin D1기인표체.결과 E2작용세포72 h후,실험조세포G0/G1기적비솔(71.76±1.78)%현저고우음성대조조(51.73±1.86)%화정상대조조(47.90±0.79)%,차이유통계학의의(P＜0.05);상대응적PI치:실험조(28.24±1.78)현저저우음성대조조(47.27±1.86)화정상대조조(52.10±0.79)비교,차이유통계학의의(P＜0.05);실험조세포내Cyclin D1기인표체수평현저저우대조조.결론 자격소재대전렬선평활기세포적생물학효응중,통과자격소수체α적개도조공료세포주기소Cyclin D1적표체,종이촉진세포적증식.
Objective To investigate the role of estrogen receptor alpha (Erα) in estradiol-induced proliferation of mouse prostatic smooth muscle cells (PSMCs) and explore a new target for benign prostazic hyperplasia (BPH). Methods Adenoviral vectors with Erα-shRNA or Ctrl-shRNA were transfected into mouse PSMCs. The cells were divided into 3 groups: experimental group ( cells transfected with pGSadeno-Erα), negative control group (cells transfected with pGSadeno-Ctrl) and normal control group (normal mouse PSMCs). The expression of Cyclin DI was detecrted by Western blotting. Cell cycle was analyzed by using flow cytometry. Results After treatment in the presence of 1 10-8 mol/L 17β-estradiol (E2) for 72 h, the percentage of cells in the G0/G1 phase was (71.76 1.78)％ in experimental group, which was significantly higher than in negative control group (51.73 ± 1.86)％ and normal control group (47.90±0.79)％, and PI in experimental group (28.24±1.78) was prominently lower than in negative control group (47.27±1.86) and normal control group (52.10±0.79). The expression level of Cyclin D1 in experimental group was conspicuously lower than in control groups. Conclusion E2 regulates the expression of Cyclin D1 via Erα in PSMCs, which promotes cell proliferation.