The role of SRC1 and SRC2 in steroid-induced SDF1 expression in normal and ectopic endometrium

Xiu Shi, Shi X, Wei Xu, Xu W, Dai HH, Hui-Hua Dai, Sun Y, Ying Sun, Xiu-Li Wang, Xiuli Wang, Wang XL
Reproduction (Cambridge, England) · 2014 · vol. 147(6) , pp. 847–853 · doi:10.1530/rep-14-0027 · PMID:24586072 · W2105021025
article OA: bronze CC0 ⤵ 8 in-corpus citations
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This study found SRC1 is necessary for estradiol-induced CXCL12 expression, while SRC2 is required for progesterone to inhibit estradiol-induced CXCL12 and monocyte chemotaxis in normal and ectopic endometrial stromal cells.

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Abstract

To compare the expression patterns of steroid receptor coactivators (SRCs) and steroid-induced stromal cell-derived factor 1 (CXCL12 (SDF1)) in normal and ectopic endometrium and to explore the roles of NCOA1 (SRC1) and NCOA2 (SRC2) in the steroid-induced CXCL12 expression in normal and ectopic endometrial stromal cells (ESCs). The NCOA1, NCOA2, NCOA3 (SRC3), and CXCL12 (SDF1)α mRNA levels in normal and ectopic endometrium were analyzed by quantitative real-time PCR. Steroid-induced CXCL12 expression was detected by the ELISA method and the chemotactic activity of conditioned supernatant to monocyte was assessed by the Boyden chamber method before and after the silencing of NCOA1 or NCOA2 with siRNA in normal and ectopic ESCs. The expression of NCOA1 and CXCL12 in ectopic endometrium was significantly greater than that in normal endometrium in the secretory phase. Progesterone (P4) was able to significantly inhibit estradiol (E2)-stimulated CXCL12 expression in normal and ectopic ESCs. The inhibitory rate of P4 in ectopic ESCs at 72 and 96 h was significantly lower than that in normal ESCs. Silencing of NCOA1 but not NCOA2 significantly reduced the E2-induced CXCL12 expression in normal and ectopic ESCs. The ability of P4 to inhibit E2-induced CXCL12 expression and monocyte chemotaxis in normal and ectopic ESCs was significantly attenuated when NCOA2 was silenced. NCOA1 plays a necessary role in E2-induced CXCL12 expression and NCOA2 is required for P4 to inhibit the E2-induced CXCL12 production in normal and ectopic endometrium.

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Condition tags

endometriosis

MeSH descriptors

Chemokine CXCL12 Endometriosis Endometrium Estradiol Nuclear Receptor Coactivator 1 Nuclear Receptor Coactivator 2 Case-Control Studies Cells, Cultured Chemokine CXCL12 Chemokine CXCL12 Chemotaxis, Leukocyte Culture Media, Conditioned Culture Media, Conditioned Endometriosis Endometriosis Endometrium Endometrium Estradiol Female Humans

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References (24)

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