| Gonocytes are the precursors of spermatogonial stem cells from which spermatozoa originate. We have shown that neonatal rat gonocytes proliferate in response to the combined action of PDGF and 17beta-estradiol (E2). The xenoestrogens Bisphenol A and genistein, previously shown to alter the male reproductive system, stimulated gonocyte proliferation through crosstalk with the PDGF pathway in a manner similar to E2, while testosterone and progesterone did not affect gonocyte proliferation. Gonocytes expressed Raf1, MEK1, ERK1/2 and PI3K, and proliferated through ERK1/2 activation. PDGF and estrogen induced rapid ERK2 phosphorylation and their combination maintained activated ERK2 for 60 minutes, localized mainly in the cytosol. E2 induced a rapid increase of estrogen receptor beta immunoreactivity in gonocyte cytosol. PDGF increased a cytosolic PDGFRbeta signal, suggesting a role for the variant V1-PDGFRbeta previously identified in gonocytes. These data suggest that PDGF and estrogen are required to maintain ERK2 activation which mediates gonocyte proliferation, and that estrogen exerts rapid non-genomic effects in gonocytes. |
