Regulation of stromal proliferation, growth arrest, differentiation and apoptosis in benign prostatic hyperplasia by TGF-beta.
This study deals with the biological role of transforming growth factor-beta (TGF-beta) in the pathogenesis of benign prostatic hyperplasia (BPH), which is a common disorder in aging males. The two known etiological factors for BPH have been the presence of testis and aging. It is well established that androgen plays an important role in the pathogenesis of BPH in aging men. The action of androgen is mediated through actions of a host of soluble growth factors, among which TGF-beta is the most versatile in its ability to regulate proliferation, growth arrest, differentiation, and apoptosis of prostatic stromal cells. It is known that BPH development involves a steady increase in the stromal compartment. A subsequent differentiation process of smooth muscle cells in the prostate is responsible for the development bladder neck obstruction secondary to BPH. However, the manner in which the testis and aging mediate the expansion in prostatic stromal compartment and the subsequent smooth muscle differentiation remains unclear. It has become increasingly apparent that TGF-beta intimately regulates the various events associated with the development of BPH. This chapter will present evidence to support the above claim (Figure 1).
Huang
Xuemei
X
Department of Urology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.
Lee
Chung
C
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D006801:Humans; D008297:Male; D011470:Prostatic Hyperplasia / Q000209:etiology* / Q000473:pathology*; D017154:Stromal Cells / Q000473:pathology; D016212:Transforming Growth Factor beta / Q000502:physiology*
D016212:Transforming Growth Factor beta