Retinoic acid suppresses interleukin-6 production in human endometrial cells

S Sawatsri, Sawatsri S, Sayan Sawatsri, Nina Desai, N. Desai, Desai N, John A. Rock, J A Rock, N Sidell, Neil Sidell, Sidell N
Fertility and sterility · 2000 · vol. 73(5) , pp. 1012–1019 · doi:10.1016/s0015-0282(00)00483-0 · PMID:10785230 · W2035523400
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This study investigated the effect of retinoic acid on human endometrial cells, finding that it suppresses interleukin-6 production.

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Abstract

OBJECTIVE: To determine whether retinoic acid (RA) can regulate the expression of interleukin (IL)-6 in human endometrial cells in a manner that might be beneficial to women with endometriosis. DESIGN: In vitro study. SETTING: Academic medical center. PATIENT(S): Patients with endometriosis and controls. INTERVENTION(S): Endometrial cell cultures were treated with RA. MAIN OUTCOME MEASURE(S): Interleukin-6 protein secretion, messenger RNA expression, and IL-6-promoter activity. RESULT(S): Using a human endometrial cell line (EM42), as well as primary stromal and epithelial endometrial cells, we demonstrated that RA suppresses IL-6 protein and messenger RNA expression in a time- and dose-dependent fashion, showing maximal effects at pharmacologically achievable blood serum concentrations (micromoles per liter). Retinoic acid specifically inhibited the activity of IL-6-promoter reporter constructs that were transiently transfected into EM42 cells. Mutational analysis of reporter constructs indicated that RA suppression of IL-6 expression was mediated, at least in part, through the nuclear factor IL-6 binding site located in the IL-6 promoter. CONCLUSION: Retinoids may play a fundamental role in altering the pathophysiology of endometriosis related to aberrant production of IL-6.

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MeSH descriptors

Endometrium Interleukin-6 Tretinoin Cells, Cultured Cells, Cultured Endometrium Endometrium Endometrium Female Female Humans Humans Interleukin-6 Interleukin-6 Phenotype Phenotype Polymerase Chain Reaction Polymerase Chain Reaction Promoter Regions, Genetic Promoter Regions, Genetic

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