17β-estradiol reduces the effect of metabolic inhibition on gap junction intercellular communication in rat cardiomyocytes via the estrogen receptor

Chung, Tun Hui; Wang, Seu Mei; Wu, Jyh‐Lin

doi:10.1016/j.yjmcc.2004.08.003

Cited by 35 publications

(28 citation statements)

References 40 publications

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“…"*"Represents P<0.05 compared to the non-17-β estradiol group; "a" represents P<0.05 compared to the non-inhibitor group; "b" represents P<0.05 towards adjacent cells. There are also researchers holding that the effect of estrogen on Cx43 might be mediated by the activation of Protein Kinase C via an ER-plasma membrane-associated signaling mechanism [62]. Besides, cells deficient in functional coupling displayed a dramatic decrease in response to PTH.…”

Section: Figurementioning

confidence: 99%

Role of Cx43-Based Gap Junction in Murine Osteoblast-Like Mc3t3-E1Cells Exposed to 17-Βestradiol

Shang¹,

Wei²,

Liang³

2017

Mol Biol

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Estrogen has garnered considerable attention because of its importance in bone mass maintenance and the efficacy of hormone therapy in combating postmenopausal osteoporosis. Gap junctions are membrane spanning protein channels present on the surfaces of adjacent cells. They enable neighboring cells to physically link, which facilitate intercellular communication by allowing passage of small molecules from cell to cell in a process known as Gap Junctional Intercellular Communication (GJIC), can make the relevant cells function as a whole. An in vitro experiment combined with microarray analyses has identified novel genes in the response of MC3T3-E1 cells to an appropriate concentration of 17-β estradiol and the results of microarray showed that gap junction alpha-1 (Gja1) in the gap junction pathway was significantly elevated. We studied the effect of 17-β estradiol on the proliferation and differentiation of MC3T3-E1 cells disrupting of GJIC among osteoblasts with the chemical inhibitor, 18α-Glycyrrhetinic Acid (AGA). And we found that an appropriate concentration and duration of 17-β estradiol increased Methyl Thiazol Tetrazolium (MTT) values, Alkaline Phosphatase (ALP) activity and Runt-related transcription factor 2 (Runx2) proteins and gene expression and facilitated the mineralization of extracellular matrix. However, the promoting effect of 17-β estradiol on the proliferation and differentiation of MC3T3-E1 cells was weakened under the action of AGA. Therefore, we suggest that 17-β estradiol promotes MC3T3-E1's proliferation, differentiation and functions associated with Cx43-based GJIC, but gap junction is not the only signaling pathway that mediates the influence of 17-β estradiol on osteoblasts. The specific regulatory mechanism has yet to be researched.

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Section: Figurementioning

confidence: 99%

Role of Cx43-Based Gap Junction in Murine Osteoblast-Like Mc3t3-E1Cells Exposed to 17-Βestradiol

Shang¹,

Wei²,

Liang³

2017

Mol Biol

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“…But little is known about the effects of estrogen on GJs in the arrhythmogenesis during the I/R process. Recent studies revealed that Cx43 is the principal ventricular coupling protein, 23 and disorganization of cytoskeletal proteins, mainly vinculin, can result in disarray of adherens junction proteins. 25-27 Cx43 exists mainly as a phosphoprotein in normal cardiomyocytes, 23 and its dephosphorylation has dramatic effects on or can reflect injury to both electrical and chemical coupling in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies revealed that Cx43 is the principal ventricular coupling protein, 23 and disorganization of cytoskeletal proteins, mainly vinculin, can result in disarray of adherens junction proteins. 25-27 Cx43 exists mainly as a phosphoprotein in normal cardiomyocytes, 23 and its dephosphorylation has dramatic effects on or can reflect injury to both electrical and chemical coupling in cardiomyocytes. 16,22,23,28 In additional, ZemljicHarpf et al 29 found that cardiac-myocyte-specific excision of the vinculin gene caused conduction abnormalities (complete AVB, ectopy, and nonsustained polymorphic VT) and high mortality rates in homozygous global vinculin knockout (cVclKO) mice; gender affected the mortality rate in cVclKO mice, with male mice showing more rapid mortality than female mice.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Estrogen Against Reperfusion Arrhythmias Following Severe Myocardial Ischemia in Rats

Wang

Zhao

et al. 2010

Circ J

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Background: Female sex hormones may have protective effects against arrhythmias, including reperfusion arrhythmias (RAs), but the mechanisms are still not completely known. Methods and Results:Serial changes in rat hearts (rhythm, apoptosis and the its infuencing factors; cardiac vinculin mRNA expression and connexin43 (Cx43) dephosphorylation) were examined during periods of ischemia-reperfusion with and without estrogen treatment. After reperfusion, although the incidence of arrhythmias became higher in both the vehicle-group and estrogen-group, compared with the ischemia period, estrogen prevented reperfusion-induced upregulation of the incidence of arrhythmias, especially ventricular premature beats (VPB) and ventricular tachycardia (VT). The duration of VT and fibrillation, and the number of VPB and VT, were all significantly decreased in the estrogen-group. The expression of cardiac vinculin mRNA decreased significantly in the vehicle-group but not in the estrogen-group. Cx43 dephosphorylation and myocyte apoptosis increased in both groups, but the values for the estrogen-group were all markedly lower than those for the vehicle-group. A selective estrogen receptor (ER) β agonist prevented reperfusion-induced upregulation of the incidence of both VPB and VT significantly; a selective ERα agonist had no significant influence. Conclusions:Estrogen can protect the heart against RAs, at least in part, mediated through gap junctions. Upregulation of ERβ but not ERα mediated most of the estrogen-induced cardioprotection against RA. (Circ J 2010; 74: 634 - 643)

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“…49 After binding E2 in the cytoplasm, and forming homo-or heterodimers, the ERs translocate to the nucleus where, by interacting with estrogen response elements, they modulate expression of peroxisome proliferator activator γ, endothelial nitric oxide synthase, connexin, and heat shock proteins genes ( Figure S1 in the online-only Data Supplement). [50][51][52][53][54] The receptor homo-or heterodimers affect gene expression also indirectly via transcription factor or via ligand-independent mechanisms involving a growth factor that induces phosphorylation of ER. 55 Membrane subpopulations of ERs deriving from the same transcripts yielding nuclear ERs, which anchor to plasma membrane lipids, 56 have been implicated in the rapid (nongenomic) estrogen signaling.…”

Section: Erα and Erβmentioning

confidence: 99%

Estrogen Signaling in the Adrenal Cortex

et al. 2016

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17β-estradiol reduces the effect of metabolic inhibition on gap junction intercellular communication in rat cardiomyocytes via the estrogen receptor

Cited by 35 publications

References 40 publications

Role of Cx43-Based Gap Junction in Murine Osteoblast-Like Mc3t3-E1Cells Exposed to 17-Βestradiol

Role of Cx43-Based Gap Junction in Murine Osteoblast-Like Mc3t3-E1Cells Exposed to 17-Βestradiol

Protective Effects of Estrogen Against Reperfusion Arrhythmias Following Severe Myocardial Ischemia in Rats

Estrogen Signaling in the Adrenal Cortex

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