Up-Regulation of Gap Junctional Intercellular Communication and Connexin43 Expression by Retinoic Acid in Human Endometrial Stromal Cells

Tanmahasamut, Prasong; Sidell, Neil

doi:10.1210/jc.2004-0663

Cited by 38 publications

(44 citation statements)

References 44 publications

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“…Levels of gap junctional intercellular communication (GJIC) in control and treated cells in culture were determined by SL/DT (Scrape Loading/Dye Transfer) technique using a fluorescent dye, Lucifer Yellow (LY) (Invitrogen, Eugene, OR) [12,13]. hSV SMCs were washed thoroughly with PBS in which Ca 2+ was omitted to prevent uncoupling of the cells.…”

Section: Scrape Loading/dye Transfermentioning

confidence: 99%

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway

Jia

Cheng

Gangahar

et al. 2008

Journal of Molecular and Cellular Cardiology

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Proliferation and migration of vascular smooth muscle cells (VSMCs) lead to intimal thickening and influence the long-term patency of venous graft post coronary arterial bypass graft. There is increasing evidence that connexins are involved in the development of intimal hyperplasia and restenosis. We assessed connexin 43 (Cx43) expression and its role in angiotensin II-induced proliferation and migration of smooth muscle cells and the signal pathways involved in human saphenous vein bypass conduits. Angiotensin-II significantly increased gap junctional intercellular communication and induced the expression of Cx43 in human saphenous vein SMCs in a dose-and time-dependent manner through angiotensin II type 1 receptor. The effect of angiotensin-II was blocked by siRNA of ERK 1/2, p38 MAPK and JNK, respectively. Overexpression of Cx43 markedly increased the proliferation of saphenous vein SMCs. However, siRNA for Cx43 inhibited angiotensin-II-induced proliferation, cyclin E expression and migration of human saphenous vein SMCs. In dual-luciferase reporter assay, angiotensin-II markedly activated AP-1 transcription factor, which was significantly attenuated by a dominant negative AP-1 (A-Fos) with subsequent inhibition of angiotensin-II-induced transcriptional expression of Cx43. These data demonstrate the role of Cx43 in the proliferation and migration of human saphenous vein SMCs and angiotensin-II induced Cx43 expression via mitogen-activated protein kinases (MAPK)-AP-1 signaling pathway.

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Section: Scrape Loading/dye Transfermentioning

confidence: 99%

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway

Jia

Cheng

Gangahar

et al. 2008

Journal of Molecular and Cellular Cardiology

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“…RA and other retinoids enhance GJIC and CX43 expression levels in numerous cell types, certain human cancer cell types, mouse fibroblasts and rat liver cells, through transcriptional and translational mechanisms (Stahl & Sies 1998, Carystinos et al 2001. When treated with RA, CX43 expression in human endometrial stromal cells shows a dose-dependent increase at the mRNA and protein levels (Tanmahasamut & Sidell 2005) (Table 2). 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).…”

Section: Gap Junction Intercellular Communicationsmentioning

confidence: 99%

“…The expression of these same genes can be modulated by ovarian steroid hormones (i.e., estradiol and progesterone) treatment (Vermot et al 2000, Li & Ong 2003, Rühl et al 2006, Fritzsche et al 2007). The retinoid pathway is known to play vital roles in endometrial development and differentiation (Tanmahasamut & Sidell 2005, Wu et al 2013, Nakajima et al 2016, as well as endometrial neovascularization (Sidell et al 2010) and blastocyst implantation (Han et al 2010, Ma et al 2012.…”

Section: Introductionmentioning

confidence: 99%

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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“…To investigate the role of HUVEC connexins on monocyte-endothelial adhesion, HUVEC were treated with oleamide, which rapidly inhibited Cx channels, including Cx43 (14), or with retinoic acid, which our previous study demonstrated increases the expression of Cx43 in these cells (15). The effects of oleamide and retinoic acid treatment on U937-HUVEC adhesion, Cx43 expression and ATP release were determined.…”

Section: Effects Of Oleamide and Retinoic Acid Treatment On The Exprementioning

confidence: 99%

Connexin 43 expressed in endothelial cells modulates monocyte-endothelial adhesion by regulating cell adhesion proteins

Yuan

Sun

Zhang

et al. 2015

Molecular Medicine Reports

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Abstract. Adhesion between circulating monocytes and vascular endothelial cells is a key initiator of atherosclerosis. In our previous studies, it was demonstrated that the expression of connexin (Cx)43 in monocytes modulates cell adhesion, however, the effects of the expression of Cx43 in endothelial cells remains to be elucidated. Therefore, the present study investigated the role of the expression of Cx43 in endothelial cells in the process of cell adhesion. A total of four different methods with distinct mechanisms were used to change the function and expression of Cx43 channels in human umbilical vein endothelial cells: Cx43 channel inhibitor (oleamide), enhancer (retinoic acid), overexpression of Cx43 by transfection with pcDNA-Cx43 and knock-down of the expression of Cx43 by small interfering RNA against Cx43. The results indicated that the upregulation of the expression of Cx43 enhanced monocyte-endothelial adhesion and this was markedly decreased by downregulation of Cx43. This mechanism was associated with Cx43-induced expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1. The effects of Cx43 in endothelial cells was independent of Cx37 or Cx40. These experiments suggested that local regulation of endothelial Cx43 expression within the vasculature regulates monocyte-endothelial adhesion, a critical event in the development of atherosclerosis and other inflammatory pathologies, with baseline adhesion set by the expression of Cx43. This balance may be crucial in controlling leukocyte involvement in inflammatory cascades.

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Up-Regulation of Gap Junctional Intercellular Communication and Connexin43 Expression by Retinoic Acid in Human Endometrial Stromal Cells

Cited by 38 publications

References 44 publications

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway

Physiological and pathological implications of retinoid action in the endometrium

Connexin 43 expressed in endothelial cells modulates monocyte-endothelial adhesion by regulating cell adhesion proteins

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