| Yeh SD |
------>authors3_c=None ------>paper_class1=2 ------>Impact_Factor=None ------>paper_class3=0 ------>paper_class2=0 ------>vol=March ------>confirm_bywho=shiemin ------>insert_bywho=yehsd ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=1 ------>paper_class2Letter=None ------>page2=39 ------>medlineContent= ------>unit=E0117 ------>insert_date=20051220 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=None ------>score=447 ------>journal_name=Program of 2005 Annual meeting and 23rd general scientific meeting of the Taiwanese Association of Andrology ------>paper_name=Infertility with defective spermatogenesis and hypotestosteronemia in male mice lacking the androgen receptor in leydig cells ------>confirm_date=20060210 ------>tch_id=091054 ------>pmid=17955388 ------>page1=39 ------>fullAbstract=Androgen and the androgen receptor (AR) have been shown to play critical roles in male fertility. Our previous data demonstrated that mice lacking AR (AR(-/y)) revealed incomplete germ cell development and lowered serum testosterone levels, which resulted in azoospermia and infertility. However, the consequences of AR loss in Leydig cells remain largely unknown. Using a Cre-LoxP conditional knockout strategy, we generated a tissue-specific knockout mouse (L-AR(-/y)) with the AR gene deleted by the anti-Mullerian hormone receptor-2 (Amhr2) promoter driven Cre expressed in Leydig cells. Phenotype analyses show that the outside appearance of L-AR(-/y) mice was indistinguishable from wild type mice (AR(+/y)), but with atrophied testes and epididymis. L-AR(-/y) mice were infertile, with spermatogenic arrest predominately at the round spermatid stage and no sperm could be detected in the epididymis. L-AR(-/y) mice also have lower serum testosterone concentrations and higher serum leuteinizing hormone and follicle-stimulating hormone concentrations than AR(+/y) mice. Further mechanistic studies demonstrated that hypotestosteronemia in L-AR(-/y) mice is not caused by reducing numbers of Leydig cells, but instead by the alterations of several key steroidogenic enzymes, including 17beta-HSD3, 3beta-HSD6, and P450c17. Together, L-AR(-/y) mice provide in vivo evidence that functional AR in Leydig cells is essential to maintain normal spermatogenesis, testosterone production, and required for normal male fertility. ------>tmu_sno=None ------>sno=12360 ------>authors2=Yeh SY ------>authors3=Lin H ------>authors4=Chang CS ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Yeh SD ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=1 ------>updateTitle=Infertility with defective spermatogenesis and steroidogenesis in male mice lacking androgen receptor in Leydig cells. ------>language=1 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2005 ------>submit_flag=None ------>publish_month=1 |