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. 2004 May;63(5):983-8.
doi: 10.1016/j.urology.2003.11.024.

Biologic feature of prostatic hyperplasia developed in spontaneously hypertensive rats

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Biologic feature of prostatic hyperplasia developed in spontaneously hypertensive rats

Xianghua Zhang et al. Urology. 2004 May.

Abstract

Objectives: To investigate alterations in cell kinetic and cellular composition in prostatic hyperplasia developed in spontaneously hypertensive (SH) rats from 15 to 54 weeks of age.

Methods: Male SH rats (n = 20) and their normotensive counterparts, Wistar-Kyoto rats (n = 20), were studied. At 15, 29, 40, and 54 weeks of age, the ventral prostate was obtained to evaluate (a) cell proliferation by the proliferation index using proliferating cell nuclear antigen immunostaining and (b) apoptosis by the apoptotic index using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling assay. The percentage of area density of smooth muscle and fibroblastic tissues was determined with a computerized image analysis system after alpha-actin and vimentin immunostaining, respectively.

Results: Compared with the data in the Wistar-Kyoto rats during the observation period, a significantly increased proliferation index in both epithelium and stroma (P <0.01) and a slightly increased apoptotic index in the epithelium without apoptotic cells in the stroma, with an imbalance in favor of cell proliferation, were noted in the prostatic hyperplasia of the SH rats. The value of the proliferation index was greatly increased in both the epithelium and the stroma of the SH rats between 15 and 29 weeks (P <0.05) but continued relatively steady from 29 to 54 weeks. A significantly increased percentage of smooth muscle area (P <0.01) and a much greater percentage of area density of smooth muscle than that of fibroblastic tissues (P <0.01) were observed in the prostatic hyperplasia of the SH rats.

Conclusions: The prostatic hyperplasia of SH rats may develop from both epithelial and stromal growth and could ultimately be promoted by an imbalance in favor of proliferative activity.

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