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Basal and interleukin-1 beta-stimulated prostaglandin production from cultured human myometrial cells: Differential regulation by corticotropin-releasing hormone

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UNSPECIFIED (1999) Basal and interleukin-1 beta-stimulated prostaglandin production from cultured human myometrial cells: Differential regulation by corticotropin-releasing hormone. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 84 (6). pp. 2204-2211.

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Abstract

During pregnancy, placental CRH acts on human myometrium via specific receptors and might play a role in the regulation of myometrial contractility and hence human parturition. The myometrium is the site of production and target of several PGs, which can be activated by cytokines, especially during infection-induced preterm labor. We established primary human myometrial cell cultures that express functional CRH receptors (CRH-R1 alpha, -R1 beta, -R1c, and -R2 beta) to investigate the possible regulation of PG production by CRH. We studied the effect of CRH on the two major myometrial PGs, PGE(2) and 6-keto PGF(1 alpha). Human CRH was able to partially inhibit basal, interleukin-1 beta-stimulated, and oxytocin-stimulated PGE(2) production (56 +/- 11%, 45 +/- 88, and 58 +/- 6% inhibition, respectively), This effect was blocked by a specific CRH receptor antagonist in a concentration-dependent manner. Furthermore, CRH had no effect on 6-keto PGF(1 alpha) production, indicating that the CRH inhibitory action does not involve suppression of cyclooxygenase, the enzyme responsible for the production of both PGE(2) and 6-keto-PGF(1 alpha). These data further support the view that during pregnancy, CRH may promote myometrial quiescence and might play an important role in the regulation of human labor.

Item Type: Journal Article
Subjects: R Medicine > RC Internal medicine
Journal or Publication Title: JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Publisher: ENDOCRINE SOC
ISSN: 0021-972X
Official Date: June 1999
Dates:
DateEvent
June 1999UNSPECIFIED
Volume: 84
Number: 6
Number of Pages: 8
Page Range: pp. 2204-2211
Publication Status: Published

Data sourced from Thomson Reuters' Web of Knowledge

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