Xia Weiliang, Mruk Dolores D, Lee Will M, Cheng C Yan
Center for Biomedical Research, Population Council, 1230 York Avenue, New York, New York 10021, USA.
J Endocrinol. 2007 Mar;192(3):563-83. doi: 10.1677/JOE-06-0158.
During spermatogenesis, extensive restructuring takes place at the Sertoli-Sertoli and Sertoli-germ cell interface, which is regulated via intriguing interactions among cytokines, proteases, protease inhibitors, kinases, phosphatases, and transcription factors. This in turn determines the steady-state levels of integral membrane proteins at the cell junctions. We sought to further expand these observations using the Adjudin model. Adjudin is a potential male contraceptive that targets Sertoli-germ cell adhesion, causing exfoliation of spermatids and spermatocytes, but not spermatogonia, from the seminiferous epithelium. This model thus provides the means to identify crucial regulatory molecules and signaling pathways pertinent to junction restructuring events during spermatogenesis. In this study, genome-wide expression profiling of rat testes after treatment with Adjudin at the time of extensive junction restructuring was performed. Differentially regulated genes, such as cytokines, proteases, protease inhibitors, cell junction-associated proteins, and transcription factors pertinent to junction restructuring were identified. These data were consistent with earlier findings; however, much new information was obtained which has been deposited at the Gene Expression Omnibus data repository website: http://www.ncbi.nih.gov/geo/ with Accession number: GSE5131. The primary signaling events pertinent to junction restructuring in the testis induced by Adjudin were also delineated using bioinformatics. These findings were also consistent with recently published reports. The identified molecular signatures or targets pertinent to junction dynamics in the testis as reported herein, many of which have not been investigated, thus offer a framework upon which the regulation of junction restructuring events at the Sertoli-Sertoli and Sertoli-germ cell interface pertinent to spermatogenesis can be further studied.
在精子发生过程中,支持细胞-支持细胞和支持细胞-生殖细胞界面会发生广泛的结构重组,这一过程通过细胞因子、蛋白酶、蛋白酶抑制剂、激酶、磷酸酶和转录因子之间有趣的相互作用来调节。这反过来又决定了细胞连接处整合膜蛋白的稳态水平。我们试图利用阿地司亭模型进一步拓展这些观察结果。阿地司亭是一种潜在的男性避孕药,它靶向支持细胞-生殖细胞黏附,导致精子细胞和精母细胞从生精上皮脱落,但不影响精原细胞。因此,该模型提供了一种手段,来识别与精子发生过程中连接结构重组事件相关的关键调节分子和信号通路。在本研究中,我们在广泛的连接结构重组时,对经阿地司亭处理的大鼠睾丸进行了全基因组表达谱分析。鉴定出了差异调节基因,如与连接结构重组相关的细胞因子、蛋白酶、蛋白酶抑制剂、细胞连接相关蛋白和转录因子。这些数据与早期的研究结果一致;然而,我们获得了许多新信息,这些信息已存于基因表达综合数据库网站:http://www.ncbi.nih.gov/geo/,登录号为:GSE5131。我们还利用生物信息学描绘了阿地司亭诱导的睾丸中与连接结构重组相关的主要信号事件。这些发现也与最近发表的报告一致。本文报道的与睾丸连接动力学相关的已鉴定分子特征或靶点,其中许多尚未被研究,因此提供了一个框架,在此基础上可以进一步研究与精子发生相关的支持细胞-支持细胞和支持细胞-生殖细胞界面连接结构重组事件的调控。