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Nadeem A. Siddiqui, Andrew Loughney, Eric J. Thomas, William Dunlop, Christopher P.F. Redfern, Cellular retinoid binding proteins and nuclear retinoic acid receptors in endometrial epithelial cells, Human Reproduction, Volume 9, Issue 8, 1 August 1994, Pages 1410–1416, https://doi.org/10.1093/oxfordjournals.humrep.a138720
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Abstract
Retinoic acid, one of the most potent of the naturally occurring retinoids (retinol and derivatives), is required in vivo for the maintenance of epithelial cell growth. This study describes the pattern of expression of nuclear retinoic acid receptors (RARs and RXRs), and cellular binding proteins for retinol and retinoic acid (CRBP I, CRABP I and II), in endometrial epithelial cells. The effects of retinoic acid on the expression of these receptors in endometrial epithelial cells have also been studied and compared with its effects in endometrial stromal cells. Messenger RNA for RAR-α, RAR-β, RAR-γ, RXR-α, CRBP I and CRABP II was detected by Northern blotting of total RNA extracted from cultured epithelial cells. In comparison with stromal cell RNA that was used as an internal standard, CRBP I appeared to be more abundant in epithelial cells, whereas CRABP II appeared to be more abundant in the stromal cells. This implies that the intracellular concentration of retinoic acid may be maintained at higher levels in epithelial cells compared to stromal cells. In addition, the response of the two cell types to retinoic acid differs: RAR-β is induced in stromal cells treated with all-trans retinoic acid but not in epithelial cells. From these data we suggest that retinoid physiology differs between endometrial epithelial and stromal cells.Furthermore, by analogy with other studies, we propose that retinoic acid may be maintained at a higher intracellular concentration in endometrial epithelial cells to facilitate differentiation to a glandular phenotype. Since RAR-β is induced by retinoic acid in endometrial stromal cells but not endometrial epithelial cells, retinoic acid may also play a role in mediating stromal-epithelial cell interactions in endometrial differentiation.
