Retinoids and spermatogenesis: Lessons from mutant mice lacking the plasma retinol binding protein

被引:65
作者
Ghyselinck, Norbert B.
Vernet, Nadege
Dennefeld, Christine
Giese, Norbert
Nau, Heinz
Chambon, Pierre
Viville, Stephane
Mark, Manuel
机构
[1] Univ Strasbourg, Coll France, IGBMC, ICS,CNRS,INSERM, F-67404 Strasbourg, France
[2] Sch Vet Med, Dept Food Toxicol, Hannover, Germany
关键词
cell proliferation; cell survival; testis; nuclear receptors; paracrine signaling; retinoic acid; spermatogonia; vitamin A deficiency;
D O I
10.1002/dvdy.20795
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Using Rbp4-null mice as models, we have established for the first time the kinetics of the spermatogenetic alterations during vitamin A deficiency (VAD). Our data demonstrate that the VAD-induced testicular degeneration arises through the normal maturation of germ cells in a context of spermatogonia differentiation arrest. They indicate that retinoic acid (RA) appears dispensable for the transition of premeiotic to meiotic spermatocytes, meiosis, and spermiogenesis. They confirm that RA plays critical roles in controlling spermatogonia differentiation, spermatid adhesion to Sertoli cells, and spermiation, and suggest that the VAD-induced arrest of spermatogonia differentiation results from simultaneous blocks in RA-dependent events mediated by RA receptory gamma (RAR gamma) in spermatogonia and by RAR alpha in Sertoli cells. They also provide evidence that expression of major RA-metabolizing enzymes is increased in mouse Sertoli cells upon VAD and that vitamin A-deficient A spermatogonia differ from their RA-sufficient counterparts by the expression of the Stra8 gene.
引用
收藏
页码:1608 / 1622
页数:15
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