open access

https://hdl.handle.net/2115/53592

Galectin-1 and galectin-3 in the corpus luteum of mice are differentially regulated by prolactin and prostaglandin F2α

英語

2012-11

Society for Reproduction and Fertility

Reproduction

144(5)

617-624

Galectin-1 and galectin-3, β-galactoside-binding lectins, are specifically expressed in the regressing corpus luteum (CL) of mice, however, their function remains unclear. In this study, we examined the effects of prolactin (PRL) and prostaglandin F2α (PGF2α), two main regulatory molecules of mouse CL function, on galectin expression. In situ hybridization analysis clearly demonstrated an initial increase in galectin-1 in the CL newly formed (CLN) after postpartum ovulation 48 h after compulsory weaning. This was accompanied by a decline in 3β-hydroxysteroid dehydrogenase (3β-HSD) and luteinizing hormone receptor (LH-R) expression, suggesting a withdrawal of PRL stimulation. At 72 h after the weaning, the expression of both galectins in CLN was remarkably increased, being associated with an intense expression of progesterone degradation enzyme (20α-HSD). Compulsory weaning did not significantly alter both galectin expression in the remaining CL of pregnancy (CLP), while PGF2α strongly up-regulated both galectin expression only in the remaining CLP which lacked LH-R in postpartum mice. Administration of Bromocriptine, an antagonist for PRL secretion, to non-pregnant cyclic mice induced an accumulation of galectin-1 - but not galectin-3 - in all CL of various generations, and additional PRL treatment reduced its accumulation, suggesting a direct suppressive effect of PRL on galectin-1 expression. Although the function and regulatory mechanism of galectin in the CL is not fully understood, PGF2α is an excellent candidate which regulates galectin expression but its effect may be abolished by LH-R-mediated signal. PRL withdrawal seems to be necessary for an initiation of luteolysis and the following PGF2α-induced galectin expression.

学術雑誌論文

Accepted Manuscript

Disclaimer. This is not the definitive version of record of this article. This manuscript has been accepted for publication in Reproduction, but the version presented here has not yet been copy edited, formatted or proofed. Consequently, the journal accepts no responsibility for any errors or omissions it may contain. The definitive version is available at http://hdl.handle.net/10.1530/REP-11-0495, 2012 Society for Reproduction and Fertility.

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