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短暂性腱生蛋白增强是大鼠前列腺雄激素去除后的早期事件。

Transient tenascin enhancement is an early event after androgen ablation in rat prostate.

作者信息

Xue Y, van der Laak J A, Latijnhouwers M A, Smedts F, van der Poel H G, de la Rosette J J, Debruyne F M, Schalken J

机构信息

Department of Urology, University Hospital Nijmegen, The Netherlands.

出版信息

Urol Res. 1999;27(1):9-15. doi: 10.1007/s002400050083.

Abstract

Tenascin (tenascin-C), a mesenchymal glycoprotein, is expressed in many tissue remodeling processes. We evaluated tenascin expression during androgen-deprivation-related involution of the rat prostate. At set intervals following castration and subsequent testosterone repletion, prostates were removed in 30 adult rats. Each prostate was immunostained with a polyclonal antiserum against rat tenascin and keratin antibodies specifically directed against exocrine basal cells and luminal cells in the prostate glandular structure. Morphologic impressions were semiquantatively evaluated using a computer-assisted image analysis system. Rat prostates showed a transient increase in the periglandular tenascin expression directly following castration that reached a maximum at day 3. At day 6, tenascin expression was similar to control prostates. This was accompanied by a decrease of cells in the luminal cell layer. The weakest tenascin immunoreactivity was noted on day 14 after androgen withdrawal. This process was reversed by androgen repletion. This study shows that in the rat prostate tenascin expression may be androgen dependent and that during androgen deprivation-related involution tenascin expression is probably associated with tissue remodeling by stromal-epithelial interactions.

摘要

腱生蛋白(腱生蛋白-C)是一种间充质糖蛋白,在许多组织重塑过程中表达。我们评估了大鼠前列腺雄激素剥夺相关退化过程中腱生蛋白的表达。在去势及随后补充睾酮后的设定时间间隔,对30只成年大鼠的前列腺进行切除。每个前列腺用抗大鼠腱生蛋白的多克隆抗血清以及特异性针对前列腺腺结构中外分泌基底细胞和管腔细胞的角蛋白抗体进行免疫染色。使用计算机辅助图像分析系统对形态学印象进行半定量评估。大鼠前列腺在去势后腺周腱生蛋白表达立即出现短暂增加,在第3天达到最大值。在第6天,腱生蛋白表达与对照前列腺相似。这伴随着管腔细胞层细胞数量的减少。雄激素撤除后第14天腱生蛋白免疫反应性最弱。该过程通过雄激素补充得以逆转。本研究表明,在大鼠前列腺中腱生蛋白表达可能依赖雄激素,并且在雄激素剥夺相关退化过程中,腱生蛋白表达可能与基质-上皮相互作用引起的组织重塑有关。

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