PMID- 7588230 OWN - NLM STAT- MEDLINE DCOM- 19951127 LR - 20131121 IS - 0013-7227 (Print) IS - 0013-7227 (Linking) VI - 136 IP - 11 DP - 1995 Nov TI - Prostaglandin F2 alpha mediates ovarian sterol carrier protein-2 expression during luteolysis. PG - 4963-72 AB - In the corpus luteum, prostaglandin F2 alpha (PGF2 alpha) appears to be a physiological agent with both antisteroidogenic and luteolytic actions. It is hypothesized that the antisteroidogenic action of PGF2 alpha acts through altered transport of cholesterol to the mitochondrial cytochrome P450 side-chain cleavage enzyme (P450scc). However, the effect of PGF2 alpha on the expression of the putative cholesterol transport protein, sterol carrier protein-2 (SCP2; 13.2 kilodaltons), has not been examined. In this study, the decline in serum progesterone after PGF2 alpha injection was examined in parallel with altered ovarian SCP2, P450scc, and 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) protein and messenger RNA (mRNA) levels. Rats (28 days old) were treated with 8 IU PMSG to induce follicular development and ovulation. Ten days after ovulation, animals were treated with PGF2 alpha (single or multiple injections; 100-250 micrograms each) or left untreated. Ovarian SCP2, P450scc, and 3 beta HSD protein and mRNA levels were examined 0 (time zero), 4, and 8 h post-PGF2 alpha treatment using Western and Northern blot analysis. SCP2 mRNA levels were also examined using a highly sensitive ribonuclease protection assay that detects a 429-base pair SCP2-mRNA specific sequence. The results indicate that serum progesterone was significantly reduced 4 and 8 h after PGF2 alpha injections (P < 0.001; n = 6/time point). The decline in progesterone paralleled a 50-60% reduction in 3 beta HSD protein and mRNA levels by 4 h post-PGF2 alpha. Protein and mRNA levels for 3 beta HSD returned to control values by 8 h post-PGF2 alpha treatment. P450scc expression was also reduced at 4 h (44-54%), but by 8 h, both protein and mRNA levels had increased above the normal control levels (P < 0.02). In contrast, the 0.8-kilobase SCP2-specific mRNA transcript was reduced to 50% and 80% of the pre-PGF2 alpha treatment level at 4 and 8 h, respectively (P < 0.01). SCP2 ribonuclease protection assay analysis also indicated that SCP2 mRNA levels were reduced 65% (P < 0.03) and 85% (P < 0.01) by 4 and 8 h post-PGF2 alpha treatment compared to those in time zero ovarian tissue. Consistent with the loss of SCP2 mRNA expression, Western blot analysis indicated that a 15-kilodalton SCP2-immunoreactive protein (presumably the pro-SCP2 form) was significantly reduced or absent in the PGF2 alpha treated animals (P < 0.04).(ABSTRACT TRUNCATED AT 400 WORDS) FAU - McLean, M P AU - McLean MP AD - Department of Obstetrics and Gynecology, University of South Florida College of Medicine, Tampa 33606, USA. FAU - Billheimer, J T AU - Billheimer JT FAU - Warden, K J AU - Warden KJ FAU - Irby, R B AU - Irby RB LA - eng GR - HD-31644/HD/NICHD NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Endocrinology JT - Endocrinology JID - 0375040 RN - 0 (Carrier Proteins) RN - 0 (Plant Proteins) RN - 0 (RNA, Messenger) RN - 0 (sterol carrier proteins) RN - 4G7DS2Q64Y (Progesterone) RN - B7IN85G1HY (Dinoprost) RN - EC 1.1.- (3-Hydroxysteroid Dehydrogenases) RN - EC 1.14.15.6 (Cholesterol Side-Chain Cleavage Enzyme) SB - IM MH - 3-Hydroxysteroid Dehydrogenases/genetics MH - Animals MH - Base Sequence MH - Blotting, Northern MH - Blotting, Western MH - Carrier Proteins/*genetics MH - Cholesterol Side-Chain Cleavage Enzyme/genetics MH - Dinoprost/*pharmacology MH - Female MH - Gene Expression/*drug effects MH - Molecular Sequence Data MH - Ovary/*metabolism MH - *Plant Proteins MH - Progesterone/blood MH - RNA, Messenger/metabolism MH - Rats MH - Rats, Sprague-Dawley EDAT- 1995/11/01 00:00 MHDA- 1995/11/01 00:01 CRDT- 1995/11/01 00:00 PHST- 1995/11/01 00:00 [pubmed] PHST- 1995/11/01 00:01 [medline] PHST- 1995/11/01 00:00 [entrez] AID - 10.1210/endo.136.11.7588230 [doi] PST - ppublish SO - Endocrinology. 1995 Nov;136(11):4963-72. doi: 10.1210/endo.136.11.7588230.