Peritubular cells may modulate Leydig cell-mediated testosterone production through a nonclassic pathway

Abstract

OBJECTIVE: To evaluate whether paracrine signals are responsible for hormone-independent Leydig cell (Lc) steroidogenesis in the testis. DESIGN: Testicular peritubular cells (PTc), Sertoli cells (Sc), and Lc were isolated and cultured, and their effect on each other was evaluated in terms of lactate production by Sc and testosterone (T) production by Lc. SETTING: Research institution. ANIMAL(S): Wistar rats. INTERVENTION(S): Testes were surgically removed, and a new, easily adoptable procedure for PTc was developed; culture media from Sc, PTc, and Lc cultures were used for treating pure populations of these cells. Cells were also cocultured together. MAIN OUTCOME MEASURE(S): To assess culture or coculture supernatants for presence of metabolites and Lc messenger RNA analysis. RESULT(S): Although PTc secreted factor(s) did not augment production of Sc lactate, essential for germ cell survival, they significantly augmented T secretion by Lc, independent of StAR gene expression. Coculture studies showed that T production by Lc was significantly stimulated when Lc were cocultured with PTc, even in the absence of hormones. CONCLUSION(S): Testicular peritubular cell-derived factor(s) can potentially augment T production by Lc in a nonclassic manner even in a gonadotropin-deficient environment.