Altered retinoid signaling compromises decidualization in human endometriotic stromal cells

Mary Ellen Pavone, Pavone ME, Saurabh Malpani, Malpani S, Matthew Dyson, Matthew T. Dyson, Serdar E. Bulun, Bulun Se
Reproduction (Cambridge, England) · 2017 · vol. 154(3) , pp. 207–216 · doi:10.1530/rep-16-0592 · PMID:28592664 · W2621844414
Lab / animal OA: closed CC0 ⤵ 10 in-corpus citations
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Decidualization in human endometrial cells alters retinoid signaling via RBP4 for paracrine effects, a pathway that is blunted in endometriotic cells, potentially explaining decidualization defects.

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Abstract

Decidualization alters multiple molecular pathways in endometrium to permit successful embryo implantation. We have reported that paracrine factors, including retinoids, secreted from progesterone-treated endometrial stromal cells, act on nearby epithelial cells to induce the estradiol metabolizing enzyme HSD17B2. This same induction is not seen in endometriotic stromal cells. We have also shown significant differences in retinoid uptake, metabolism and action in endometriotic tissue and stromal cells compared to normal endometrium. Here, we characterize retinoid signaling during decidualization in these cells. Endometrial and endometriotic cells were isolated, cultured and incubated and decidualized. Genes involved in retinoid metabolism and trafficking were examined using RT-PCR and Western blotting. Prolactin, a decidualization marker, was also examined. We found that both endometrial and endometriotic stromal cells express all intracellular proteins involved in retinoid uptake and metabolism. Decidualization significantly reduced the expression of the genes responsible for retinoid uptake and shuttling to the nucleus. However, expression of CRBP1, an intracellular carrier protein for retinol, increased, as did RBP4, a carrier protein for retinol in the blood, which can function in a paracrine manner. Secreted RBP4 was detected in the media from decidualized endometrial cells but not from endometriotic cells. We believe that retinoid trafficking in endometrial stromal cells during decidualization may shift to favor paracrine rather than intracrine signaling, which may enhance signaling to the adjacent epithelium. There is blunting of this signaling in endometriotic cells. These alterations in retinoid signaling may help explain the decidualization defects and deficient estradiol inactivation (via HSD17B2) seen in endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Decidua Endometrium Fatty Acid-Binding Proteins Receptors, Retinoic Acid Retinoids Retinol-Binding Proteins, Plasma Stromal Cells Adult Adult Cell Movement Cell Movement Cells, Cultured Cells, Cultured Decidua Decidua Decidua Embryo Implantation Embryo Implantation Endometrium Endometrium

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (43)

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