Effects of Estrogen on PCNA Expression in Rat Uterus

• Main Authors: Hsiao, Li-Der, 蕭立德
• Other Authors: Ling-Ru Lee
• Format: Others
• Language: zh-TW
• Published: 1996
• Online Access: http://ndltd.ncl.edu.tw/handle/55510314071684207668

碩士 === 國立成功大學 === 生理學研究所 === 84 === My study is aimed at delineating﹀he cellular and nuclear mechanisms throughwhich estrogen stimulate DNA synthesis and cell proliferation in the uterus.I focus on the proliferating cell nuclear antigen (PCNA) which is expressedin cell nuclei just before the S-phase and serves to activate DNA replication. First, I examined specimens of rat uteri taken at each stage of the estrouscycle and using immunocytochemical staining procedures to observe the appearanceand histological distribution of PCNA among the tissues of these specimens.I found that at diestrus I and II, PCNA expression was detected predominatelyin the glandular and luminal epithelia of the endometrium. At proestrus, PCNA staining in the glandular and luminal epithelial cells decreased, whilePCNA positive cells appeared strongly in the stromal cells and also in the myometrium. By the day of estrus, staining in the glandular and luminal epitheliawas reduced sharply. Then, the role of estrogen on these events was investigated by ovariectomy (OVX) and by replacement estradiol (E2) treatment. By 10 days after OVX, the PCNA positive cells were decreased markedly in stromaltissue elements and even more so in the luminal epithelia. In cotrast, PCNA staining in the glandular epithelia was hardly affected. By 12 days after OVX, PCNA stained cells were rarely observed. Two weeks after OVX, PCNA expression was virtually abolished. When OVX rats were treated with E2, PCNA positive cells were observed in the glandular and luminal epithelia. Although this study is still in progress, the results can be summarized as follows. (1) PCNA is expressed periodically in the uterus in synchrony with the estrous cycle. (2) The differential responses of rat uterus luminal and glandular epithelial cellsto OVX indicate that the estrogen effect on endometrial proliferation may notoccur by means of a single, homogenous regulatory mechanism.