The expression of retinoic acid receptors in cultured human endometrial stromal cells and effects of retinoic acid

Andrew, P. D.; Matthews, Craig J.; Thomas, Eric J.; Redfern, Christopher P.F.

doi:10.1093/oxfordjournals.humrep.a137721

Cited by 14 publications

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“…RA then diffuses into the adjacent epithelium, where it is catabolized by CYP26A1 induced by progesterone during the late secretory phase or implantation. Numerous studies demonstrated the expression of RARs and RXRs in human endometrial epithelial and stromal cells (Prentice et al 1992, Kumarendran et al 1996, Fukunaka et al 2001. Using Northern blot, Kumarendran et al (1996) demonstrated that RARβ mRNA expression is 1.7-fold higher in epithelial samples from the proliferative phase than from the secretory phase.…”

Section: Hormonal Control Of Endometrial Retinoid Pathwaymentioning

confidence: 99%

“…Concomitant with the increase in CX43 expression, stromal cells treated with RA exhibit a 2.5-fold enhancement in their GJIC as assessed by dye transfer experiments (Tanmahasamut & Sidell 2005). The ability of endometrial stromal cells to serve as an RA-responsive target is supported by the presence of RA nuclear receptors (i.e., RARs and RXRs) in these cells (Prentice 1992, Comptour et al 2016. In addition to its expression level, the phosphorylation status of CX43 influences GJIC, including gap junction assembly and channel gating (Solan & Lampe 2009).…”

Section: Gap Junction Intercellular Communicationsmentioning

confidence: 99%

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Physiological and pathological implications of retinoid action in the endometrium

Jiang

Chen

Taylor

et al. 2018

Journal of Endocrinology

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Retinol (vitamin A) and its derivatives, collectively known as retinoids, are required for maintaining vision, immunity, barrier function, reproduction, embryogenesis and cell proliferation and differentiation. Despite the fact that most events in the endometrium are predominantly regulated by steroid hormones (estrogens and progesterone), accumulating evidence shows that retinoid signaling is also involved in the development and maintenance of the endometrium, stromal decidualization and blastocyst implantation. Moreover, aberrant retinoid metabolism seems to be a critical factor in the development of endometriosis, a common gynecological disease, which affects up to 10% of reproductive age women and is characterized by the ectopic localization of endometrial-like tissue in the pelvic cavity. This review summarizes recent advances in research on the mechanisms and molecular actions of retinoids in normal endometrial development and physiological function. The potential roles of abnormal retinoid signaling in endometriosis are also discussed. The objectives are to identify limitations in current knowledge regarding the molecular actions of retinoids in endometrial biology and to stimulate new investigations toward the development potential therapeutics to ameliorate or prevent endometriosis symptoms.

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