Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

We studied steroidogenesis and the regulation of Leydig cell-specific gene expression in primary cultures of highly purified postnatal fetal Leydig cells (PFLCs). PFLCs activated by hCG and (Bu)2cAMP demonstrated transient capacity to produce testosterone (T) in vitro. A time dependent decline in T production by (Bu)2cAMP-stimulated PFLCs was observed and associated with the accumulation of progesterone in the culture media and complete suppression of P450c17 expression at the translational but not transcriptional level. PFLCs was found to lose their capacity to express Leydig cell-related genes (e.g., 3βHSD, P450c17, Insl3), which was restored by treatment with (Bu)2cAMP. It was also found that PDGFα alone and in combination with (Bu)2cAMP significantly stimulated proliferation of the isolated PFLCs in vitro. Our data indicate that cAMP-activated signaling pathway(s) play an important role in the regulation of PFLC differentiation and function.

► Postnatal fetal Leydig cells (PFLCs) have a transient capacity to produce testosterone. ► Long-term culturing of PFLCs attenuates the expression of steroidogenic genes. ► Treatment with (Bu)2 cAMP restores steroidogenic genes expression in PFLC. ► PDGFa and cAMP-PKA signaling stimulates the proliferation of PFLCs.