GENE-EXPRESSION OF PANCREATIC-TYPE PHOSPHOLIPASE-A2 IN RAT OVARIES - STIMULATORY ACTION ON PROGESTERONE RELEASE

We reported previously that pancreatic-type group I phospholipase-A2 (PLA(2)-I) stimulates DNA synthesis or prostaglandin E(2) production in various cell types via its specific receptors on the cell surface. In the present study we examined the effect of PLA(2)-I on corpus luteum, which possesses specific PLA(2)-I receptors, and demonstrated gene expression of PLA(2)-I in rat ovaries. PLA(2)-I stimulated progesterone release from incubated corpora lutes at concentrations above 10 nM in a dose-dependent manner. Northern blot analysis revealed the presence of PLA(2)-I messenger RNA (mRNA) in rat ovaries. The level of PLA(2)-I mRNA was elevated during diestrus to proestrus, and decreased to almost nothing on the day of estrus. To further evaluate the timing of PLA(2)-I expression, we analyzed RNAs extracted from small follicles, large preovulatory follicles, and corpora lutea obtained from various phases of hCG-treated immature rats. During follicular development, mRNA levels remained negligible. The level of PLA(2)-I mRNA began to rise after luteinization of follicles and increased during the maturation of the corpora lutea. Levels of PLA(2)-I mRNA in ovaries from day 5 and day 10 pregnant rats were 5- to 10-fold higher than those in diestrous rats, whereas on day 21, the mRNA level was decreased. Immunocytochemical studies were performed to clarify the synthesis and localization of PLA(2)-I in the ovary using polyclonal anti-PLA(2)-I antibodies. Intense immunoreactivity was detected only in luteal cells of newly formed corpora lutea. However, the number and intensity of immunoreactive cells decreased in old corpora lutea. No immunoreactivity was detected in follicular cells of small- or middle-sized follicles. These results demonstrate the correlation among PLA(2)-I gene expression, estrous cycle, and progesterone secretion in rat ovaries and suggest a new function of PLA(2)-I as an intragonadal regulatory factor for steroidogenesis.