摘要
为研究雌激素促进前列腺间质细胞增殖的机理,使用雌二醇(E2)或BSA雌二醇(BSA-E2)处理前列腺间质细胞系wpmy-1,用MTT法及细胞计数法检测细胞增殖情况;用实时RT-PCR以及Western印迹方法检测细胞增殖核抗原(PCNA)的表达水平;用抗磷酸化ERK1/2抗体检测细胞内MAPK途径的激活情况.结果显示,2种形式的雌二醇均能促进前列腺间质细胞系wpmy-1的增殖,并且显著上调增殖相关核抗原PCNA的表达水平;2种形式的雌激素均能快速激活wpmy-1细胞内的MAPK信号通路;MAPK途径的特异性抑制剂PD98059能够显著降低雌激素对细胞增殖以及PCNA表达水平的上调作用.结果表明,雌激素能够通过膜受体快速激活前列腺间质细胞中的MAPK信号通路,进而促进前列腺间质细胞的增殖.
To investigate the mechanism of estrogen treatment on promoting the proliferation in prostatic stromal cells, a prostatic stromal cell line, wpmy-1, was stimulated with different concentrations of estradiol （E2） or BSA-estradiol （BSA-E2）. Cell proliferation was monitored by MTT assay and cell counting, and the level of proliferating cell nuclear antigen （PCNA） was measured by real-time RT-PCR and Western blotting. The phosporylation of ERK1/2, an indicator of the activation of MAPK pathway was also determined by Western blotting. We found both E2 and BSA-E2 up- regulated the proliferation of wpmy-1 cells and the expression level of PCNA. We also observed a rapid activation of the MAPK pathway following E2 and BSA-E2 treatments in wpmy-1 cells. The increase of cell proliferation and PCNA expression induced by estrogen was significantly blocked by PD98059, a selective inhibitor of MAPK pathway. We postulate that estrogen could activate MAPK pathway through its membrane receptor and up-regulate the cell proliferation in prostatic stroma cells.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2008年第2期153-159,共7页
Chinese Journal of Biochemistry and Molecular Biology
基金
国家自然科学基金(No.30471733,30672101,30600218)
国家自然科学基金国际交流与合作项目(两个基地项目No.30410403237)
天津市自然科学基金(No.05YFJMJC07300)~~
