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Biology of Reproduction 62, 1121-1127 (2000)
© 2000 Society for the Study of Reproduction, Inc.


Articles

Secretion and Gene Expression of Metalloproteinases and Gene Expression of Their Inhibitors in Porcine Corpora Lutea at Different Stages of the Luteal Phase1

Lutz Pitzel2,a, Sabine Lüdemanna, and Wolfgang Wuttkea

a Clinical and Experimental Endocrinology, Department of Obstetrics and Gynecology, University of Göttingen, 37075 Göttingen, Germany

We hypothesize that spontaneous regression of corpora lutea (CL) involves short-lasting restructure of luteal tissue with an activation of matrix metalloproteinases (MMPs) and their respective inhibitors (tissue inhibitors of metalloproteinase, TIMPs). This was tested by determining the gene expression of MMP-1, MMP-2, and MMP-9 and respective TIMP-1 and TIMP-2 in luteal tissue from sows at the early, midluteal, and late luteal phase (Days 6–8, Days 9–11, and Days 13–15 of estrous cycle). Gene expression of the three MMPs was low in early, slightly higher in midluteal, and significantly elevated (P < 0.05) in regressing CL. An inverse pattern was found for gene expression of TIMP-1 and TIMP-2. Under culture conditions, the release of MMPs was determined from steroidogenic large luteal cells (LLC). LLC harvested from regressing CL released significantly (P < 0.05) more active MMPs than cells obtained from CL at the early luteal phase. As luteolysis can be induced by prostaglandin F2{alpha} (PGF2{alpha}) and tumor necrosis factor {alpha} (TNF), we studied their effects on LLC under culture conditions. Treatment of cells with PGF2{alpha} or TNF (10-7 M or 3 x 10-9 M, respectively) induced a significantly higher release of MMPs, and gene expression was also significantly stimulated in comparison to that in untreated LLC. The gene expression of TIMPs remained unaffected by either treatment. It is concluded that at the beginning of luteolysis, MMPs are expressed and released in high amounts and that this is essential for the structural regression of the CL.

First decision: 1 November 1999.

1 This study was generously funded by the German Research Society (DFG Grant No. Wu 60/10-3).

2 Correspondence: L. Pitzel, Division of Clinical and Experimental Endocrinology, Department of Obstetrics and Gynecology, University of Göttingen, Robert-Koch-Strasse 40, D-37075 Göttingen/Germany. FAX: 551 396518; ufkendo{at}med.uni-goettingen.de




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