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Trans-Differentiation of Prostatic Stromal Cells Leads to Decreased Glycoprotein Hormone Production

Austrian Academy of Sciences (H.R., G.U., K.M., P.B.), Institute for Biomedical Aging Research, Innsbruck A6020, Austria; Ludwig Boltzmann Institute for Andrology and Urology (E.P.), Hospital Lainz, Vienna A1130, Austria; and Institute of Medical Chemistry and Biochemistry (M.H.), Leopold-Franzens-University of Innsbruck, Innsbruck A6020, Austria

Address all correspondence and requests for reprints to: Peter Berger, Ph.D., Austrian Academy of Sciences, Institute for Biomedical Aging Research, Peter Mayr Strasse 4b, Innsbruck, A6020, Austria. E-mail: peter.berger{at}oeaw.ac.at.

Abstract

Age-related development of benign prostatic hyperplasia is an important health issue in developed countries. The histopathogenetic hallmark of this disease is the increase in relative and absolute numbers of smooth muscle cells (SMC). Glycoprotein hormone -subunit (GPH) is expressed in the human prostate, and, because of its structural similarities to other cystine knot growth factors, it has been considered to have growth regulatory functions of its own. Primary cell cultures allowing for selective cultivation of prostatic epithelial cells, fibroblasts, and SMC were established. Directed trans-differentiation and cellular homogeneity was pursued by confocal scanning laser microscopy with cell type-specific markers. GPH production by these cells was assessed by immunofluorimetric assays. Its predominant source was young fibroblasts, whereas replicative senescent fibroblasts, SMC, and control fibroblasts from foreskin did not produce significant amounts. Functionally, GPH reduced growth of stromal cells at concentrations of 10 and 100 nmol/liter as shown by cell viability assays. It is concluded that histogenetic reorganization over the adult lifetime, guided by endocrine factors like steroid hormones together with senescence of fibroblasts, leads to a decreased production of growth inhibitors, such as GPH, favoring proliferation and the development of benign prostatic hyperplasia.

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