Issue |
Reprod. Nutr. Dev.
Volume 43, Number 6, November-December 2003
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Page(s) | 517 - 525 | |
DOI | https://doi.org/10.1051/rnd:2004006 |
DOI: 10.1051/rnd:2004006
Opposite regulation of clusterin and LH receptor in the swine corpus luteum during luteolysis
Monica Forni, Augusta Zannoni, Carlo Tamanini and Maria Laura BacciDepartment of Veterinary Morphophysiology and Animal Production, University of Bologna, Via Tolara di Sopra, 50, 40064 Ozzano Emilia (BO), Italy
Received 20 June 2003; accepted 20 September 2003
Abstract -
Luteolysis, 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 (PGF
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.
Key words: LH receptor / tissue growth / clusterin / apoptosis / luteolysis
Corresponding author: Monica Forni mforni@vet.unibo.it
© INRA, EDP Sciences 2003