Inhibitory role of REV-ERBα in the expression of bone morphogenetic protein gene family in rat uterus endometrium stromal cells

Tasaki, Hirotaka; Zhao, Lijia; Isayama, Keishiro; Chen, Huatao; Yamauchi, Nobuhiko; Shigeyoshi, Yasufumi; Hashimoto, Seiichi; Hattori, Masa Aki

doi:10.1152/ajpcell.00220.2014

Cited by 16 publications

(9 citation statements)

References 71 publications

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“…5B). The Bmp2 transcript, selected as a positive control, was also upregulated by SR8278 treatment, as previously reported (50). Concomitantly, the production of PGE 2 significantly increased at 24 h after treatment with the antagonist (P Ͻ 0.01 vs. CONT; Fig.…”

Section: Expression Levels Of Clock Genes and Ptgs2 In The Pregnant Rsupporting

confidence: 77%

Removal of Rev-erbα inhibition contributes to the prostaglandin G/H synthase 2 expression in rat endometrial stromal cells

Isayama

Zhao

Chen

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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The rhythmic expression of clock genes in the uterus is attenuated during decidualization. This study focused on Ptgs2, which is essential for decidualization, as a putative clock-controlled gene, and aimed to reveal the functions of clock genes in relation to Ptgs2 during decidualization. We compared the transcript levels of clock genes in the rat uterus on days 4.5 (D4.5) and 6.5 of pregnancy. The transcript levels of clock genes (Per2, Bmal1, Rorα, and Rev-erbα) had decreased at implantation sites on day 6.5 (D6.5e) compared with those on D4.5, whereas Ptgs2 transcripts had increased on D6.5e. Similar observations of Rev-erbα and Ptgs2 were also obtained in the endometrium on D6.5e by immunohistochemistry. In the decidual cells induced by medroxyprogesterone and 2-O-dibutyryl-cAMP, the rhythmic expression levels of clock genes were attenuated, whereas Ptgs2 transcription was induced. These results indicate that decidualization causes the attenuation of clock genes and the induction of Ptgs2. Furthermore, in the experiment of Bmal1 siRNA, the rhythmic expression of clock genes and Ptgs2 was attenuated by the siRNA. Transcript levels of Ptgs2 and prostaglandin (PG)E₂ production were increased by treatment with the Rev-erbα antagonist, suggesting the contribution of the nuclear receptor Rev-erbα to Ptgs2 expression. Moreover, Rev-erbα knockdown enhanced the induction of Ptgs2 transcription and PGE₂ production by forskolin. Chromatin immunoprecipitation-PCR analysis revealed that Rev-erbα could directly bind to a proximal RORE site of Ptgs2. Collectively, this study demonstrates that the attenuation of the circadian clock, especially its core component Rev-erbα, contributes to the induction of Ptgs2 during decidualization.

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Section: Expression Levels Of Clock Genes and Ptgs2 In The Pregnant Rsupporting

confidence: 77%

Removal of Rev-erbα inhibition contributes to the prostaglandin G/H synthase 2 expression in rat endometrial stromal cells

Isayama

Zhao

Chen

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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“…Meanwhile, BMAL1 regulation of TGF-β and BMP signaling in the control of fat adipogenesis has also been reported (27). a recent study showed that BMal1 silencing-induced BMP2 was found in rat uterus endometrium stromal cells (28). Samsa et al (5) recently reported that BMal1 -/mice had reduced osteoblast differentiation in vitro and they proposed some potential molecular mechanism of BMal1-dependent control of osteogenic differentiation including oxidative stress response, the mTor signaling pathway and translation.…”

Section: Discussionmentioning

confidence: 89%

Icariin promotes osteogenic differentiation of BMSCs by upregulating BMAL1 expression via BMP signaling

Huang

Wei

et al. 2020

Mol Med Report

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increasing research has demonstrated that expression of brain and muscle arnT-like 1 (BMal1) and other circadian clock genes can be regulated by drugs and toxicants. We previously demonstrated that icariin, extracted from Herba epimedii, sromotes osteogenic differentiation. However, the mechanism underlying the association between icariin and BMal1 in osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMScs) remains unclear. The present study was designed with an aim to clarify the association between icariin and BMal1 in osteogenic differentiation of BMScs. The cell counting Kit-8 assay was used to evaluate cell proliferation. The expression of bone morphogenetic protein 2 (BMP2), runX family transcription factor 2 (runX2), alkaline phosphatase (alP), osteocalcin (oc) and BMal1 in BMScs was evaluated by reverse transcription-quantitative Pcr and western blotting. alP and alizarin red S (arS) staining were also performed. icariin promoted BMSc proliferation, and upregulated expression of osteogenic genes and BMal1. in addition, expression of the osteogenic genes BMP2, runX2, alP and oc were upregulated by BMal1 overexpression. Furthermore, we confirmed that BMal1 deficiency suppressed osteogenic differentiation in BMScs. Finally, arS staining of BMal1 -/-BMScs revealed that BMal1 was an essential intermediary in matrix mineralization during osteogenic differentiation. in conclusion, these results demonstrated that icariin promoted osteogenic differentiation through BMal1-BMP2 signaling in BMScs. The present study thus described a novel target of icariin that has potential applications in the treatment of osteogenic disorders.

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“…The involvement of REV-ERBα was also implicated in the molecular control of decidualization. Evidence supports an inverse role of REV-ERBα on bone morphogenetic proteins (BMPs) in rat uterus endometrial stromal cells (UESCs); in Bmal1 siRNA-transfected UESCs, the Rev-erbα was downregulated and, consequently, Bmp2, Bmp4, and Bmp6 genes were upregulated [21]. The same investigators also observed that growth/differentiation factor (Gdf) 10 and 15 and prostaglandin G/H synthase 2 (Ptgs2), which are significantly increased during decidualization, were only upregulated after Rev-erbα was downregulated.…”

Section: The Uterine Biological Rhythm As a Target For Melatonin's Acmentioning

confidence: 99%

“…Sci. 2020,21, 300 11 of This figure illustrates possible mechanisms by which melatonin influences endometriosis (EMS). It is well-accepted that elevations in mitochondrial NAS/melatonin ratio, E2 levels, and ROS formation are associated with EMS development; other conditions like pinealectomy and circadian clock disruption are also reported to suppress melatonin which may possibly enhance the risk of EMS.…”

mentioning

confidence: 99%

Melatonin Promotes Uterine and Placental Health: Potential Molecular Mechanisms

Chuffa

Lupi

Cucielo

et al. 2019

IJMS

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The development of the endometrium is a cyclic event tightly regulated by hormones and growth factors to coordinate the menstrual cycle while promoting a suitable microenvironment for embryo implantation during the “receptivity window”. Many women experience uterine failures that hamper the success of conception, such as endometrium thickness, endometriosis, luteal phase defects, endometrial polyps, adenomyosis, viral infection, and even endometrial cancer; most of these disturbances involve changes in endocrine components or cell damage. The emerging evidence has proven that circadian rhythm deregulation followed by low circulating melatonin is associated with low implantation rates and difficulties to maintain pregnancy. Given that melatonin is a circadian-regulating hormone also involved in the maintenance of uterine homeostasis through regulation of numerous pathways associated with uterine receptivity and gestation, the success of female reproduction may be dependent on the levels and activity of uterine and placental melatonin. Based on the fact that irregular production of maternal and placental melatonin is related to recurrent spontaneous abortion and maternal/fetal disturbances, melatonin replacement may offer an excellent opportunity to restore normal physiological function of the affected tissues. By alleviating oxidative damage in the placenta, melatonin favors nutrient transfer and improves vascular dynamics at the uterine–placental interface. This review focuses on the main in vivo and in vitro functions of melatonin on uterine physiological processes, such as decidualization and implantation, and also on the feto-maternal tissues, and reviews how exogenous melatonin functions from a mechanistic standpoint to preserve the organ health. New insights on the potential signaling pathways whereby melatonin resists preeclampsia and endometriosis are further emphasized in this review.

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Inhibitory role of REV-ERBα in the expression of bone morphogenetic protein gene family in rat uterus endometrium stromal cells

Cited by 16 publications

References 71 publications

Removal of Rev-erbα inhibition contributes to the prostaglandin G/H synthase 2 expression in rat endometrial stromal cells

Removal of Rev-erbα inhibition contributes to the prostaglandin G/H synthase 2 expression in rat endometrial stromal cells

Icariin promotes osteogenic differentiation of BMSCs by upregulating BMAL1 expression via BMP signaling

Melatonin Promotes Uterine and Placental Health: Potential Molecular Mechanisms

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