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pubmed-article:15141436pubmed:abstractTextLuteolysis, which occurs in a cyclical way to remove luteal tissue, may be an example of physiological apoptosis which counterbalances rapid tissue growth after ovulation. Clusterin is a multifunctional glycoprotein expressed in different tissues undergoing apoptosis. In this study we investigated clusterin and LH receptor gene expression during luteolysis as potential regulators of tissue growth and regression. Luteolysis was induced in pregnant sows (45 days) by Cloprostenol (PGF2 alpha analogue) treatment. Clusterin expression increased in the corpora lutea of pregnant sows ovariectomized 0, 6, 12, 24, 48 or 72 (n = 3) h after the luteolytic stimulus; maximum values were observed 24-48 h after the treatment (P < 0.01). An opposite trend between clusterin mRNA expression and markers of luteal function, such as progesterone levels in the corpora lutea and plasma, and LHr mRNA expression levels, was observed; moreover, clusterin expression was positively correlated with the degree of genomic DNA fragmentation, a marker of occurring apoptosis (P < 0.01). This pattern may be important in regulating luteolysis by a switch between luteotrophic and apoptotic stimulus. Our data indicate that P4 levels decrease prior to the increase in clusterin mRNA and the drop in LHr mRNA expression; we may therefore hypothesize a split between functional and structural luteolysis as reported in other species.lld:pubmed
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pubmed-article:15141436pubmed:pagination517-25lld:pubmed
pubmed-article:15141436pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:15141436pubmed:articleTitleOpposite regulation of clusterin and LH receptor in the swine corpus luteum during luteolysis.lld:pubmed
pubmed-article:15141436pubmed:affiliationDepartment of Veterinary Morphophysiology and Animal Production, University of Bologna, Via Tolara di Sopra, 50, 40064 Ozzano Emilia, BO, Italy. mforni@vet.unibo.itlld:pubmed
pubmed-article:15141436pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15141436pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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