Editorial:Molecular EndocrinologyArticles in the Spotlight for December 2013

Abstract

Welcome to the December issue of Molecular Endocrinology. Among this month’s papers you’ll find the following research to be of great interest, particularly to those interested in reproductive biology. “ATF3 Expression in the Corpus Luteum: Possible Role in Luteal Regression” by Mao et al shows that the luteolytic hormone prostaglandin F2 (PGF2 ) selectively stimulated the expression of activating transcription factor 3 (ATF3) mRNA and ATF3 protein in large steroidogenic cells of the bovine corpus luteum in vivo and in vitro. The action of PGF2 was associated with the rapid activation of stress-activated protein kinases and the induction of ATF3 in large luteal cells. Furthermore, expression of ATF3 in large or small steroidogenic cells reduced LH-stimulated cAMP response element (CRE)mediated transcription downstream of protein kinase A (PKA) signaling and inhibited progesterone synthesis at a step before conversion of cholesterol to progesterone. Therefore, ATF3 may be primarily responsible for the PGF2 -dependent reduction in steroid synthesis that occurs during luteal regression. In “COUP-TFII Regulates Human Endometrial Stromal Genes Involved in Inflammation,” Li et al demonstrate that chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) was spatially and temporally expressed in endometrial stroma cells during the menstrual cycle in women. Furthermore, COUP-TFII was found to be reduced in stroma cells of ectopic lesions in endometriosis patients. Cistromic and transcriptomic analyses demonstrated that COUP-TF regulated processes critical for human endometrial stroma cell decidualization in vitro. Specifically, COUP-TFII was responsible for the down-regulation of inflammatory genes during decidualization. This may contribute to the function of decidual stroma cells in pregnancy and the pathology observed in endometriosis. In “BMP15 Suppresses Progesterone Production by Down-regulating StAR via ALK3 in Human Granulosa Cells” (freely available at http://mend.endojournals.org/), Chang et al found that bone morphogenetic protein 15 (BMP15), but not growth differentiation factor 9 (GDF9), reduced basal progesterone production by suppressing the expression of the rate-limiting steroidogenic regulatory (StAR) protein. Neither affected the expression of cytochrome P450 side chain cleavage (P450scc) enzyme or 3 -hydroxysteroid dehydrogenase (3 -HSD). The authors also showed that knockdown of ALK2 dramatically decreased basal StAR levels, indicating a positive role for ALK2 in maintaining StAR expression. Therefore, these findings suggest that oocyte-derived BMP15 plays a role in preventing premature luteinization by modulating progesterone production during the late stage of follicle development. Congratulations to all the authors in this issue for their fine work and research. Donald B. DeFranco, PhD Editor-in-Chief, Molecular Endocrinology