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Myosin heavy chain gene expression in normal and hyperplastic human prostate tissue

Benign prostatic hyperplasia (BPH) is common among aging men. Over 80% of males 50–60 years and older have various degrees of bladder outlet obstruction secondary to BPH. Despite the tremendous medical impact of BPH, its molecular pathophysiology remains unclear. Current BPH research focuses on steroid hormonal effects, stromal‐epithelial cell interaction, and oncogenes and growth factors. But little is known about the potential prostatic smooth muscle (SM) alterations that may occur during stromal hyperplasia.