Anti-estrogen ICI 182.780 and anti-androgen flutamide induce tyrosine phosphorylation of cortactin in the ectoplasmic specialization between the Sertoli cell and spermatids in the mouse testis
Anti-estrogen ICI 182.780 and anti-androgen flutamide induce tyrosine phosphorylation of cortactin in the ectoplasmic specialization between the Sertoli cell and spermatids in the mouse testis
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DOI：
10.1016/j.bbrc.2006.05.125
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发表时间：
2006-07-21
影响因子：
3.1
通讯作者：
Mori, C
中科院分区：
文献类型：
--
作者：
Anahara, R;Toyama, Y;Mori, C
我们之前的研究表明，抗雌激素的ICI 182.780 （ICI）和抗雄激素的氟他胺（FLUT）治疗小鼠睾丸的外质特化（ES）被删除。此外，在小鼠睾丸中，氟FLUT治疗降低了一种f -肌动蛋白结合蛋白的表达。研究表明，接触蛋白可促进睾丸ES的肌动蛋白聚合，同时接触蛋白的酪氨酸磷酸化可诱导肌动蛋白解聚。本研究发现，外源性的ICI和FLUT处理导致小鼠睾丸顶端ES的皮质蛋白缺失和酪氨酸磷酸化皮质蛋白的增加。这些结果表明，性激素拮抗剂ICI和FLUT可诱导小鼠睾丸肌动蛋白解聚和酪氨酸磷酸化。同时，本研究也为阐明外源化合物对精子受精的不利影响提供了一个关键。(c) 2006爱思唯尔公司版权所有。
Our previous study revealed that the ectoplasmic specialization (ES) was deleted by the treatment of anti-estrogen, ICI 182.780 (ICI), and anti-androgen, flutamide (FLUT) in mouse testis. Also, expression of cortactin, an F-actin-binding protein, was decreased by the treatment of FLUT in mouse testis. Cortactin has been suggested to promote actin polymerizer at the ES in the testis, and also actin depolymerization is induced by tyrosine phosphorylation of cortactin. The present study revealed that exogenous treatment of ICI and FLUT caused the deletion of the cortactin in the apical ES and the increase of tyrosine phosphorylated cortactin in mouse testis. These results suggest that the sex hormone antagonists', ICI and FLUT, induced actin depolymerization and tyrosine phosphorylation of cortactin in the mouse testis. Also, the present study may be a key to elucidate the adverse affect exogenous compounds that affect spermiation. (c) 2006 Elsevier Inc. All rights reserved.