|
Comment |
Cyclic GMP dependent protein kinase II is induced by LH and PR dependent mechanisms in granulosa cells and cumulus oocyte complexes of ovulating follicles Sriraman V, et al .
Cyclic GMP dependent protein kinase II (Prkg2, cGK II) was identified as a potential target of the progesterone receptor (nr3c3) in the mouse ovary based on microarray analyses. To document this further, the expression patterns of cGK II and other components of the cGMP signaling pathway were analyzed during follicular development and ovulation using the PMSG-hCG-primed immature mice. Levels of cGK II mRNA were low in ovaries of immature mice, increased 4-fold in response to PMSG and 5-fold more within 12 h after hCG, the time of ovulation. In situ hybridization localized cGK II mRNA to granulosa cells and cumulus oocyte complexes of periovulatory follicles. In progesterone receptor null mice, cGK II mRNA was reduced significantly at 12 h after hCG in contrast to heterozygous littermates. In primary granulosa cell cultures cGK II mRNA was induced by PMA, enhanced by adenoviral expression of PR-A and blocked by RU486 and trilostane. PR-A in the absence of PMA was insufficient to induce cGK II. Expression of cGK I (Prkg1) was restricted to the residual tissue and not regulated by hormones. Guanylate cyclase-A (Npr1; GC-A)) mRNA expression increased 6-fold by 4 h after hCG treatment in contrast to PMSG alone and was localized to granulosa cells of preovulatory follicles. Collectively, these data show for the first time that cGK II (not cGK I) and GC-A are selectively induced in granulosa cells of preovulatory follicles by LH- and PR-dependent mechanisms thereby providing a pathway for cGMP function during ovulation.
|