Abstract
Increased proliferation but decreased steroidogenic capacity in Leydig cells from mice lacking cyclin-dependent kinase inhibitor 1B
Lin,Han; Hu,Guo-Xin; Dong,Lei; Dong,Qiang; Mukai,Motoko; Chen,Bing-Bing; Holsberger,Denise R.; Sottas,Chantal M.; Cooke,Paul S.; Lian,Qing-Quan; Li,Xiao-Kun; Ge,Renshan
Biology of Reproduction 80(6): 1232-1238
Publication date: 2009
Proliferating cells express cyclins, cell cycle regulatory proteinsthat regulate the activity of cyclin-dependent kinases (CDKs).The actions of CDKs are regulated by specific inhibitors, thecyclin-dependent kinase inhibitors (CDKIs), which are comprisedof the Cip/Kip and INK4 families. Expression of the Cip/KipCDKI 1B (Cdkn1b, encoding protein CDKN1B, also called p27)in developing Leydig cells (LCs) has been reported, but thefunction of CDKN1B in LCs is unclear. The goal of the presentstudy was to determine the effects of CDKN1B on LC proliferationand steroidogenesis by examining these parameters in Cdkn1bknockout (Cdkn1b) mice. LC proliferation was measured byBrdU incorporation. Testicular testosterone levels, mRNA levelsand enzyme activities of steroidogenic enzymes were comparedin Cdkn1b and Cdkn1b mice. The labeling index(LI) of LCs in Cdkn1b mice was 1.5 ± 0.2%, almost 7-fold higher than 0.2 ± 0.08 % (P < 0.001)in the Cdkn1b control mice. LC number per testis in Cdkn1bmice was two-fold that seen in the Cdkn1b control mice. However,testicular testosterone levels, mRNA levels of steroidogenicacute regulatory protein (Star), cholesterol side-chain cleavageenzyme (Cyp11a1) and 3beta-hydroxtsteroid dehydrogenase 6 (Hsd3b6)and their respective proteins were significantly lower in Cdkn1bmice. We conclude that deficiency of Cdkn1b increased LC proliferationbut decreased steroidogenesis. Thus, Cdkn1b is an importantregulator of LC development and function.
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