Transforming growth factor-beta elicits shape changes and increases contractility of testicular peritubular cells.

Testicular peritubular cells (PC) in culture in serum-rich Eagle's minimal essential medium (MEM) on a polystyrene substratum proliferate and form fibroblast-like monolayers. The cells assume a flattened shape, and F-actin microfilaments are assembled to form prominent stress fibers. When PC grown under these conditions are dispersed and replated at a low density, a subsequent shift from serum-rich MEM to serum-free MEM results in dramatic changes. Within an hour, the cells round up, the F-actin microfilament assemblies, together with the cytoskeleton, become disrupted, and the degree of contractility is diminished. Under these conditions, addition of transforming growth factor-beta (TGF-beta) results in a more rapid recovery than that observed in cells maintained in basal MEM alone. The presence of TGF-beta results in an increased percentage of cells with flattened shapes during periods between 1 and 6 h after the shift to serum-free MEM. Concomitantly, PC treated with TGF-beta form and maintain well-organized, prominent stress fibers composed of F-actin microfilament bundles. In addition, the degree of contractility of PC embedded in collagen gels and cultured in serum-free MEM is markedly enhanced in cells stimulated by TGF-beta. Treatment of cells with dibutyryl cyclic adenosine 3',5'-monophosphate (dbcAMP) or catecholeamines results in a rounding up of PC in culture, associated with a disruption of microfilament assemblies. Addition of TGF-beta prevents these effects of dbcAMP and beta-agonists, and permits PC to contract. We discuss the physiological significance of observations presented, consider possible mechanisms of action of TGF-beta on PC, and put forward the hypothesis that TGF-beta is one of the paracrine factors in the seminiferous tubule that influence interactions between Sertoli cells and peritubular myoid cells.