[Show abstract][Hide abstract] ABSTRACT: Bladder outlet obstruction (BOO) is primarily a stromal disease. Smooth muscle cells are the major cellular components of stroma. Estrogen may directly stimulate Bladder Neck smooth muscle cells (BSMC). However, little information has been gathered on the mechanism of how the estrogen affects the BSMC in vitro. The purpose of this paper is to investigate the effect of 17beta-estradiol (E(2)) on the proliferation and apoptosis of Bladder Neck Smooth Muscle Cells (BSMC) and the potential mechanisms via cell cycle analysis and related protein detection.
The synthetic rat BSMC were obtained through the enzyme-digesting method and exposed to gradient concentrations (0.1-100 nmol/l) of E(2) for different amounts of time. The progression of cell cycle, the apoptosis and the expressions of Cyclin D1 protein were examined by flow cytometry. Apoptosis-related proteins, Bcl-2 and Bax, were detected by western blot.
E(2) in the definite concentrations (0.1-10 nmol/l) promoted the BSMC growth in a concentration-dependent manner by accelerating cell cycle transition from G(1) to S phases, and up-regulating the expression of Cyclin D1. However, high doses of E(2) (10 and 100 nmol/l) increased the rate of apoptosis of the cells accompanied by a significant raise of Bax expression and the ratio of Bax/Bcl-2.
The effect of E(2) on subcultured BSMC is bilateral; it promotes the cells proliferation by enhancing the expression of Cyclin D1, which accelerates G(1) to S phase transition, while on the other hand, it induces apoptosis of the cells by up-regulating the expression of Bax.
World Journal of Urology 11/2008; 27(2):241-8. DOI:10.1007/s00345-008-0333-5 · 2.67 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Abundant evidence indicates that estrogens have an important role in the pathology of benign prostatic hyperplasia (BPH). To investigate the effect of 17β-estradiol (E2) on the proliferation and apoptosis of prostatic smooth muscle cells (PSMCs), rat PSMCs were obtained and exposed to gradient concentrations (0.1–100 nmol/l) of E2 over varying amounts of time. The progression of cell cycle, cellular apoptosis, cyclin D1, Bcl-2 and Bax proteins were detected. The data show that the effect of E2 on rat PSMCs is bilateral: it promotes cell proliferation by enhancing the expression of cyclin D1, which accelerates G1 to S phase transition; on the other hand, it induces apoptosis of the cells by up-regulating the expression of Bax. We thus suggest that an increase in estrogen may exert a launching effect in the pathology of BPH.
Cell Biology International 05/2008; 32(8-32):899-905. DOI:10.1016/j.cellbi.2008.03.023 · 1.93 Impact Factor