| Introduction and ObjectiveBenign prostatic hyperplasia (BPH) is the most common prostatic disease in elderly men. Lots of studies have investigated the possible roles of gonadal hormones, growth factors and stromal-epithelial cell interactions in prostate growth and differentiation. Some studies have indicated that several growth factors such as insulin-like growth factor- II (IGF- II), bFGF and TGF-βcan induce proliferation or aptosis in prostatic cells through secretion, leading to hyperplasia of the prostate. Cell senescence is a natural phenomenon happening in normal human body and was first oberseved in cultured cells. These cells have lost their proliferative capacity and their capacity to undergo apoptosis, however, they remain metabolically active in a growth arrested state at the G1 phase of the cell cycle. Cell senescence can prevent human cells form over-proliferation, thus it's important for suppression of oncogenesis. When PH is at 6.0, only the senescent cells can be seen as beta-galactosidase (β-gal) staining positive. Meanwhile, the morphology and functions of the senescent cells are different from normal cells. Several studies have indicated that Senescent cells accumulate in tissues with age and show changes in function, including increased expression of cytokines and proteases and decreased expression of protease inhibitors, all of which may alter the function of adjacent cells. Studies have showed that senescent cells also accumulate in the aging prostate, however, until recently, only a few studies have been devoted to investigated the functional change of this type of cells. IGF- II is a potent mitogenic factor, studies showed that expression of IGF- II in the prostate of older Wistar rats is 8.3 fold higher than that of younger rats; another study demonstrated that expression of IGF-II is several fold higher when cultured prostatic cells reached senescentce. Given that cellular senescence is associated with increased cytokine expression and BPH is strongly associated with aging. We sought to determine if cellular senescence might account for the increased expression of IGF- II in BPH tissue.Material and method30 patients with BPH undergone suprapubic prostatectomy were chosen in this study. All patients were free of carcinoma and prostatitis. Prostate tissue section were staining for IGF-II,IGF-IIR andβ-gal. Double-staining of IGF-II andβ-gal was performed in the same section. Enzyme-Linked Immunoabsorption Assay (ELISA) method was used to determine the IGF- II concentration in tissue extracts. Quantitativeβ-gal assay was used to assess tissueβ-gal activity. The relation between these two indexes was analyzed lately. Patient's age and prostate weight were then added to assess their correlation withβ-gal activity and IGF- II concentration.ResultsBoth Prostatic Epithelial and stroma Cells were staining positive for IGF- II and IGF- IIR, but IGF- II was more prominent in epithelial cells, while IGF- IIR was more obvious in stroma cells. Senescence only existed in epithelial cells, positive staining was multi-centre. Double-staining showed that positive epithelial cells contained two color particles. Statistic analysis showed that the correlation between IGF-II concentration andβ-gal activity were strongly positive (r=0.757, p = 0.001) and statistically significant. Patient's age were significantly correlating with IGF-II concentration andβ-gal activity (r=0.656 and 0.483, respectively). Prostate weight were also significantly correlating with IGF- II concentration andβ-gal activity (r= 0.820 and 0.836, respectively). Conclusions1. Accumulation of prostatic senescence epithelial cells can induce prostatic hyperplasia through excessively secreting IGF- II.2. Patient's age and Prostate weight were both significantly correlating with IGF- II concentration andβ-gal activity.
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