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Potential role for peroxisome proliferator-activated receptor in regulating luteal lifespan in the rat

Department of Animal Science, Iowa State University, Ames, Iowa 50011, USA

Correspondence should be addressed to C Komar; Email: ckomar{at}iastate.edu

Peroxisome proliferator-activated receptor (PPAR) has been shown to stimulate progesterone production by bovine luteal cells. We previously reported higher expression of PPAR in old compared with new luteal tissue in the rat. The following studies were conducted to determine the role of PPAR in rat corpora lutea (CL) and test the hypothesis that PPAR plays a role in the metabolism of progesterone and/or luteal lifespan. Ovaries were removed from naturally cycling rats throughout the estrous cycle, and pseudopregnant rats. mRNA for PPAR and P450 side-chain cleavage (SCC) was localized in luteal tissue by in situ hybridization, and protein corresponding to PPAR and macrophages identified by immunohistochemistry. Luteal tissue was cultured with agonists (ciglitazone, prostaglandin J₂) or an antagonist (GW-9662) of PPAR. Progesterone was measured in media by RIA and levels of mRNA for 20-hydroxysteriod dehydrogenase (HSD) and bcl-2 were measured in luteal tissue after culture by RT-PCR. An inverse relationship existed between the expression of mRNA for SCC and PPAR. There was no effect of PPAR agonists or the antagonist on luteal progesterone production in vitro, or levels of mRNA for 20-HSD. PPAR protein was localized to the nuclei of luteal cells and did not correspond with the presence of macrophages. In new CL, ciglitazone decreased mRNA for bcl-2 on proestrus, estrus, and metestrus. Interestingly, GW-9662 also decreased mRNA for bcl-2 on proestrus and diestrus in old and new CL, and on metestrus in new CL. These data indicate that PPAR is not a major player in luteal progesterone production or metabolism but may be involved in regulating luteal lifespan.