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热应激对连接相关分子和雄激素受体表达上游因子和猴睾丸支持细胞的影响 |
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Effect of heat stress on expression of junction-associated molecules and upstream factors androgen receptor and Wilms' tumor 1 in monkey sertoli cells |
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Chen M., Cai H., Yang J.-L., Lu C.-L., Liu T., Yang W., Guo J., Hu X.-Q., Fan C.-H., Hu Z.-Y., Gao F., Liu Y.-X. 2009/5/29 18:38:57 |
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Endocrinology, 2008, Volume 149, Issue 10
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Sertoli cells are important in determining the fate of spermatogenic cells by providing nutrition and structural support via cell junctions. In this study, we sought to examine the effect of 43 C warming on cell junctions in seminiferous epithelium and the expression of junction-associated molecules in Sertoli cells. Electron microscopy showed the appearance of large vacuoles between Sertoli and germ cells and adjacent Sertoli cells, leading to disruption of corresponding cell junctions 24 h after terminating the heat treatment. Using primary Sertoli cells isolated from pubertal monkey testes, we demonstrated that expression of adherens junction-associated molecules, such as N-cadherin and β-catenin, and tight junction-associated molecule zonula occludens protein 1 was significantly reduced in 24-48 h after heat treatment. In contrast, intermediate filament vimentin expression was up-regulated in 6-48 h. Androgen receptor (AR) and Wilms' tumor gene 1 expression dramatically decreased after heat treatment. Both proteins completely disappeared immediately after terminating heat treatment and began to recover after 6 h. Treatment of the monkey Sertoli cells with an AR antagonist, flutamide, could mimic the heat-induced changes in the expression of junction-associated molecules in Sertoli cells. Furthermore, overexpression of AR in the Sertoli cells up-regulated the expression of N-cadherin, β-catenin, and zonula occludens protein 1 and down-regulated vimentin expression. Their expression after heat treatment could be rescued by the AR overexpression. These results indicate that the decreased AR expression after heat treatment is involved in heat-induced cell junction disruption. Copyright © 2008 by The Endocrine Society. |
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Correspondence Address: Liu, Y.-X.; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China; email: liuyx@ioz.ac.cn |
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疾病资源中心
王燕燕 王曙
上海交通大学附属瑞金医院内分泌科
患者,女,69岁。2009年1月无明显诱因下出现乏力,当时程度较轻,未予以重视。2009年3月患者乏力症状加重,尿色逐渐加深,大便习惯改变,颜色变淡。4月18日入我院感染科治疗,诉轻度头晕、心慌,体重减轻10kg。无肝区疼痛,无发热,无腹痛、腹泻、腹胀、里急后重,无恶性、呕吐等。入院半月前于外院就诊,查肝功能:ALT 601IU/L,AST 785IU/L,TBIL 97.7umol/L,白蛋白 41g/L,甲状腺功能:游离T3 30.6pmol/L,游离T4 51.9pmol/L,心电图示快速房颤。
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