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Enhancement of trypsin-induced contraction by in vivo treatment with 17beta-estradiol and progesterone in rat myometrium.

ABSTRACT: We have previously reported that the contractile response to thrombin and trypsin was enhanced in the pregnant rat myometrium. We herein determined whether or not sex hormones contribute to this enhancement and the expression of protease-activated receptors (PARs). The nonpregnant rats received daily injections of either 17beta-estradiol or progesterone, and then the contractile response of the myometrium was examined ex vivo. Treatment with either 17beta-estradiol or progesterone had almost no significant enhancing effect on the high K(+)- or oxytocin-induced contraction. On the other hand, both 17beta-estradiol and progesterone dose-dependently enhanced the contractile response to trypsin. A maximal enhancement was obtained at 25 and 40 mg kg weight(-1) day(-1) for 17beta-estradiol and progesterone, respectively. The extent of the enhancement of the trypsin-induced contraction seen in the sex hormone-treated rats in the present study was comparable to that reported in the pregnant rats. However, the contractile response to thrombin and PAR1/PAR2-AP, SFLLRNP was not enhanced either by progesterone or 17beta-estradiol. PAR2-AP and PAR4-AP failed to induce contraction under any conditions. PAR1 mRNA was scarcely detected in the control myometrium by an RT-PCR analysis, while it slightly increased only in the progesterone-treated rats. Neither PAR2 nor PAR4 mRNA was detected. We thus conclude that the responsiveness to trypsin, but not thrombin, is controlled by sex hormones. A novel type of receptor, other than PAR1, PAR2 or PAR4, is suggested to mediate the trypsin-induced contraction as in the case of the pregnant rat myometrium.

SUBMITTER: Aman M

PROVIDER: S-EPMC1576290 | biostudies-literature | 2005 Oct

REPOSITORIES: biostudies-literature

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Enhancement of trypsin-induced contraction by in vivo treatment with 17beta-estradiol and progesterone in rat myometrium.

Aman Murasaki M Hirano Katsuya K Nishimura Junji J Nakano Hitoo H Kanaide Hideo H

British journal of pharmacology 20051001 3

We have previously reported that the contractile response to thrombin and trypsin was enhanced in the pregnant rat myometrium. We herein determined whether or not sex hormones contribute to this enhancement and the expression of protease-activated receptors (PARs). The nonpregnant rats received daily injections of either 17beta-estradiol or progesterone, and then the contractile response of the myometrium was examined ex vivo. Treatment with either 17beta-estradiol or progesterone had almost no ...[more]

PMID: 16056237

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Project description:The myometrium is an important reproductive tissue composed primarily of smooth muscle cells. Contractility of the myometrial smooth muscle cells during pregnancy and labour is modulated by hormones. Despite much research, little is known about the molecular mechanism by which estrogen and progesterone regulate myometrial contractility. This study investigates global gene expression profile of cultured human uterine smooth muscle cells (hUtSMCs) following 17Î²-estradiol (E2) and/or progesterone treatments using cDNA microarray technology. Furthermore the effects of addition of the progesterone inhibitor RU486 were investigated. Many genes were regulated in the presence of P4 or E2 alone but almost six times these numbers were regulated in the presence of the combination. The majority of these genes returned to near baseline levels (control samples) on addition of RU486. In total 796 annotated genes were significantly differentially expressed in the combined presence of P4 and E2 (relative to untreated levels). Furthermore, 666 annotated genes were significantly regulated by the addition of RU486 to the P4/E2 combination (relative to P4/E2 levels). Gene ontology analysis of these differentially expressed genes revealed a strong association of P4/E2 treatment with the downregulated expression of genes involved in cell communication, signal transduction, channel activity, inflammatory response and differentiation. Upregulated processes included cell survival (anti-apoptosis), gene transcription, steroid hormone biosynthesis, muscle development, insulin receptor signaling and cell growth. Functional withdrawal of progesterone using RU486 effectively reversed the processes induced by P4/E2 treatment. The hUtSMC system is an additional useful model to investigate steroid effects on smooth muscle cells in isolation from other myometrial cell types. In this study human myometrial smooth muscle cells (hUtSMCs) purchased from Lonza were cultured and treated with 17beta estradiol and progesterone either alone or in combination. In addition the 17beta estradiol and progesterone combined treated samples were also treated with the progesterone inhibitor RU486 (mifepristone). RNA was isolated after 72h from both treated and untreated control cells. The experiment was repeated 3 times. Please note that slides were scanned three times successively (i.e. 3 .gpr files per sample) and the median raw values were used as input raw data for GeneSpring analysis (Median_Table_InputRAW.xlsx).

Dataset Information

Enhancement of trypsin-induced contraction by in vivo treatment with 17beta-estradiol and progesterone in rat myometrium.

Publications

Enhancement of trypsin-induced contraction by in vivo treatment with 17beta-estradiol and progesterone in rat myometrium.

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