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Prostaglandin E-2 (PGE(2)) is a testicular peritubular cell-derived factor involved in human testicular homeostasis

机译:前列腺素E-2(PGE(2))是睾丸梗死细胞衍生因子,涉及人类睾丸稳态

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In man, blockage of prostaglandin (PG)-production e.g. by non-steroidal anti-inflammatory drug (NSAIDs) may have negative testicular side effects, implying beneficial actions of PGs in the testis. We examined human testicular samples and isolated human testicular peritubular cells (HTPCs) to explore sites of PG-synthesis and targets. HTPCs express cyclooxygenase 1 (COX1) and secrete PGE(2). Receptors (EP1, 2, 4) were specifically identified in peritubular cells. In HTPCs PGE(2) significantly increased mRNA levels of the contractility protein calponin, but did not induce contractions. PGE(2), as well as EP1 and EP4 receptor agonists, significantly increased glia cell line derived neurotrophic factor (GDNF) mRNA and/or protein levels. Importantly, the NSAID ibuprofen reduced PGE(2) and this action also lowered SMA and calponin mRNA levels and levels of secreted GDNF protein. The results reveal an unknown PGE(2) system in the human testis, in involving peritubular cells, which may be prone to interference by NSAIDs. (C) 2018 Elsevier B.V. All rights reserved.
机译:在人类中,堵塞前列腺素(PG) - 制作生产。通过非甾体抗炎药(NSAID)可能具有阴性睾丸副作用,暗示睾丸中PGS的有益作用。我们检查了人类睾丸样品和分离的人睾丸梗塞细胞(HTPC)以探索PG合成和靶点的遗址。 HTPCS表达环加氧基酶1(COX1)和分泌PGE(2)。在梗死细胞中特别鉴定受体(EP1,2,4)。在HTPCS PGE(2)中显着增加了收缩性蛋白Calponin的mRNA水平,但没有诱导收缩。 PGE(2)以及EP1和EP4受体激动剂,显着增加了胶质细胞系衍生的神经营养因子(GDNF)mRNA和/或蛋白质水平。重要的是,NSAID布洛芬降低了PGE(2),该动作还降低了SMA和Calponin mRNA水平和分泌的GDNF蛋白水平。结果揭示了人类睾丸中未知的PGE(2)系统,涉及梗死细胞,其可能易于通过NSAIDs干扰。 (c)2018 Elsevier B.v.保留所有权利。

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