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Submitted on June 28, 2004
Accepted on September 22, 2004
Departments of Obstetrics and Gynecology and Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI 48109
* To whom correspondence should be addressed. E-mail: kmjmenon{at}umich.edu.
Down-regulation of LH/hCG receptor (LHR) mRNA in the ovary following the preovulatory LH surge or the administration of a pharmacological dose of LH/hCG occurs through a post-transcriptional mechanism. A LHR mRNA binding protein (LRBP) was identified as the LHR mRNA destabilizing factor and its identity was established as mevalonate kinase (Mvk). In the present study, we determined that in the pseudopregnant rat ovary, LHR mRNA levels began to fall 4 h after hCG injection, at which time Mvk protein levels were elevated and this elevation was preceded by an increase in Mvk mRNA levels. When the cytosolic fractions of hCG treated ovaries were subjected to RNA electrophoretic mobility shift analysis, an increase in LHR mRNA-LRBP complex formation was observed, in parallel with the increase of Mvk expression. We also found that hCG coordinately up-regulated the expression of Mvk and other sterol responsive element (SRE) containing cholesterol biosynthesis enzymes, such as HMG-CoA synthase, HMG-CoA reductase and farnesyl pyrophosphate synthase. This up-regulation was transient, but the hCG induced ovarian cholesterol depletion lasted for more than 24 h. Taken together, our results suggest that in the ovary, LH/hCG up-regulates the expression of cholesterol biosynthesis enzymes as well as lipoprotein receptors to replenish cellular cholesterol, and the up-regulation of Mvk leads to a down-regulation of LHR and suppresses the LH/hCG signal cascade transiently. Thus Mvk, an enzyme involved in cholesterol biosynthesis, serves as a link between LHR mRNA expression and cellular cholesterol metabolism.
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