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Original Articles

Regulation of laminin chain gene expression by ovarian steroid hormones in uterine tissues of ovariectomized mice

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Pages 115-121 | Received 07 Dec 1996, Accepted 17 Feb 1997, Published online: 22 Nov 2010
 

Abstract

To precisely analyze the role of ovarian steroids in the regulation of laminin chain gene expression in mouse uterine tissues, the ovariectomized mouse model was used. Ovariectomized mice received a single injection of steroid hormones and total RNA was isolated from whole uterine tissues. Messenger RNA levels of each laminin chain (A, B1, and B2) were determined by competitive RT‐PCR procedures. Estradiol decreased mRNA levels of laminin B1 chain about two‐fold, and B2 chain rather moderately. Estradiol‐induced inhibition of laminin B1 and B2 chain mRNA levels were completely blocked by pretreatment with estrogen receptor antagonist tamoxifen. Estriol, a short acting estrogen which cannot induce hyperplastic responses of rodent uterine tissues, also showed an inhibitory effect on B1 and B2 chain mRNA levels, while estrone, an inactive estrogen, failed to influence either B chain mRNA levels. Effects of steroids on A chain mRNA level were quite different from those on B chains. Laminin A chain mRNA level was slightly increased by estradiol treatment, but negatively affected by progesterone. Progesterone treatment greatly increased both B chain mRNA levels, but slightly decreased A chain mRNA level compared to the control. The effect of progesterone on laminin chain‐specific mRNA levels was further increased by co‐injection of estradiol in a time‐dependent manner. Progesterone‐induced B1 and B2 chain mRNA transcription was inhibited by RU486, a synthetic anti‐progesterone/anti‐glucocorticoid. The present study demonstrates for the first time that steroids are able to regulate laminin gene expression in mouse uterine tissues, indicating that steroid‐regulated laminin gene expression is involved in uterine growth and probably differentiation.

Notes

To whom correspondence should be addressed. Tel: 82–2–880–6694, Fax: 82–2–872–1993

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