ArticleWorld journal of urology2009
17Beta-estradiol affects the proliferation and apoptosis of rat bladder neck smooth muscle cells by modulating cell cycle transition and related proteins.
Article in World journal of urology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 3 citations in OpenAlex.
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundBladder 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.
methodsThe 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.
resultsE(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.
conclusionThe 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.
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