Involvement of fas antigen in ovarian follicular atresia and luteolysis
Involvement of fas antigen in ovarian follicular atresia and luteolysis
复制标题
fas抗原参与卵巢卵泡闭锁和黄体溶解
DOI：
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发表时间：
1997
影响因子：
2.5
通讯作者：
S. Yonehara
中科院分区：
文献类型：
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作者：
K. Sakamaki;H. Yoshida;Y. Nishimura;S. Nishikawa;N. Manabe;S. Yonehara
Fas抗原（Fas）是介导细胞凋亡诱导信号的细胞表面受体蛋白，在免疫系统中起重要作用。Fas mRNA不仅在淋巴器官中表达，而且在肝脏、心脏和卵巢中也有表达。在卵巢中，细胞凋亡被认为是导致卵泡闭锁和黄体溶解的原因。我们已经调查了Fas在这些事件中的参与情况。在这里，我们报告，Fas蛋白表达的颗粒细胞和黄体细胞，但不对卵母细胞在卵巢。向成年小鼠注射具有凋亡诱导活性的抗Fas单克隆抗体可增强卵泡闭锁和黄体溶解。注射后，黄体消失，含有固缩颗粒细胞的卵泡数量增加。排卵的卵子也较少，黄体细胞产生的孕酮水平也较低。此外，由于非功能性Fas/Fas配体系统，小鼠突变型lpr（淋巴细胞增殖）的成熟卵巢在卵泡发育方面存在组织学异常，其中次级卵泡数量显著增加。这些结果提示Fas在成年小鼠卵泡闭锁和黄体溶解的生理过程中起重要作用。摩尔Reprod. Dev. 47：11-18，1997.© 1997 Wiley利斯公司
The Fas antigen (Fas) is a cell‐surface receptor protein that mediates apoptosis‐inducing signals and plays an important role in the immune system. Significant amounts of Fas mRNA can be detected not only in lymphoid organs but also in the liver, heart, and ovary. In the ovary, apoptosis is thought to cause follicular atresia and luteolysis. We have investigated the involvement of Fas in these events. Here we report that Fas protein is expressed on granulosa and luteal cells but not on oocytes in the ovary. An injection of anti‐Fas monoclonal antibody with apoptosis‐inducing activity into adult mice enhanced follicular atresia and luteolysis. After the injection, the corpora lutea disappeared and the number of follicles containing pyknotic granulosa cells increased. There were also fewer ovulated ova and lower levels of luteal cell‐produced progesterone. Furthermore, as the result of a non‐functional Fas/Fas ligand system, mature ovaries from the mouse mutant lpr (lymphoproliferation) were histologically abnormal in terms of follicular development, in that the number of secondary follicles significantly increased. These results suggested that Fas plays an important role in follicular atresia and luteolysis in the ovarian physiology of adult mice. Mol. Reprod. Dev. 47:11–18, 1997. © 1997 Wiley‐Liss, Inc.
影响因子：
3.6
作者：
S. Quirk;R. Cowan;S. Joshi;K. Henrikson;K. Henrikson
通讯作者：
S. Quirk;R. Cowan;S. Joshi;K. Henrikson;K. Henrikson
影响因子：
4.4
作者：
Rie Watanabe‐Fukunaga;C. Brannan;N. Itoh;S. Yonehara;N. Copeland;N. Jenkins;S. Nagata
通讯作者：
Rie Watanabe‐Fukunaga;C. Brannan;N. Itoh;S. Yonehara;N. Copeland;N. Jenkins;S. Nagata
影响因子：
32.4
作者：
LYNCH, DH;WATSON, ML;SELDIN, MF
通讯作者：
SELDIN, MF