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a Department of Biology, Trinity University, San Antonio, Texas 78212
b Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030
c Department of Gynecology and Obstetrics, Kyoto University Faculty of Medicine, Kyoto, Japan
Mammalian ovulation is a dynamic process that requires degradation of the collagenous connective tissue in the thecal layers of a mature follicle. In this reverse transcription-polymerase chain reaction differential display study, gonadotropin-primed immature rats were used to detect ovarian expression of a relatively new type of disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS-1) that is known to cleave extracellular matrix in acutely inflamed tissues. Immature Wistar rats were primed with 10 IU eCG s.c., and the temporal pattern of expression of the ADAMTS-1 gene was delineated by extracting ovarian RNA at 0, 2, 4, 8, 12, and 24 h after induction of ovulation by injecting the primed animals with 10 IU hCG s.c. The differential display data, Northern analyses, and in situ hybridization micrographs all showed significant up-regulation of ADAMTS-1 gene expression by 8 h after hCG administration. The in situ data indicated that the ADAMTS-1 mRNA was in the granulosa layer of mature follicles. Expression reached a peak at 12 h and remained elevated at 24 h after hCG. ADAMTS-1 gene expression was impaired by the antiprogesterone agent epostane, but this inhibition could be overcome by exogenous progesterone. ADAMTS-1 expression was not affected when ovulation was blocked by treatment of the animals with the anti-eicosanoid agent indomethacin. In conclusion, the temporal pattern of expression of this gene, and its apparent regulation by progesterone, suggests that ADAMTS-1 has a significant role in the inflammatory events of the ovulatory process.
1 This work was presented at the 32nd Annual Meeting of the Society for the Study of Reproduction held at Pullman, Washington, during the summer of 1999.
2 Supported by NSF Grant #9870793 (L.L.E.), by a Grant from The Lalor Foundation, Providence, Rhode Island (L.L.E.), and by NIH Grant HD-16229 (J.S.R.).
3 Correspondence. FAX: 210 999 7229; lespey{at}trinity.edu
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