Connexin 43 hemichannel regulates H9c2 cell proliferation by modulating intracellular ATP and [Ca&amp;lt;sup&amp;gt;2&amp;lt;/sup&amp;gt;&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt;]

Song, Dongli; Liu, Xiaoyu; Liu, Rujiao; Yang, Ling; Zuo, Jidong; Liu, Wen

doi:10.1093/abbs/gmq047

Cited by 46 publications

(36 citation statements)

References 63 publications

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“…Through GJs, the adjacent cells are engaged in the exchanging of information and material, in addition to electrical and metabolic coupling (32). It is known that GJs have important regulatory effects in VSMC proliferation, vascular tone and blood pressure (33–36). However, the association between the expression of Cxs on resistant arterioles and the development of hypertension remains to be fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Enhanced expression of Cx43 and gap junction communication in vascular smooth muscle cells of spontaneously hypertensive rats

Wang

Liu

Zhang

et al. 2016

Molecular Medicine Reports

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Niflumic acid (NFA) is a novel gap junction (GJ) inhibitor. The aim of the present study was to investigate the effect of NFA on GJ communication and the expression of connexin (Cx) in vascular smooth muscle cells (VSMCs) of mesenteric arterioles of spontaneously hypertensive rats (SHR). Whole-cell patch clamp recording demonstrated that NFA at 1×10–4 M significantly inhibited the inward current and its effect was reversible. The time for charging and discharging of cell membrane capacitance (Cinput) reduced from 9.73 to 0.48 ms (P<0.05; n=6). Pressure myograph measurement showed that NFA at 3×10-4 M fully neutralized the contraction caused by phenylephrine. The relaxation responses of normotensive control Wistar Kyoto (WKY) rats were significantly higher, compared with those of the SHRs (P<0.05; n=6). Western blot and reverse transcription-quantitative polymerase chain reaction analyses showed that the mRNA and protein expression levels of Cx43 of the third-level branch of mesenteric arterioles of the SHRs and WKY rats were higher, compared with those of the first-level branch. The mRNA and protein expression levels of Cx43 of the primary and third-level branches of the mesenteric arterioles in the SHRs were higher, compared with those in the WKY rats (P<0.05; n=6). The mRNA levels of Cx43 in the mesenteric arterioles were significantly downregulated by NFA in a concentration-dependent manner (P<0.01; n=6). The protein levels of Cx43 in primary cultured VSMCs isolated from the mesenteric arterioles were also significantly downregulated by NFA in a concentration-dependent manner (P<0.01; n=6). These results showed that the vasorelaxatory effects of GJ inhibitors were reduced in the SHRs, which was associated with a higher protein expression level of Cx43 in the mesenteric arterioles of the SHRs. NFA also relaxed the mesenteric arterioles by reducing the expression of Cx43, which decreased blood pressure. Therefore, regulation of the expression of GJs may be a therapeutic target for the treatment of hypertension.

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Section: Discussionmentioning

confidence: 99%

Enhanced expression of Cx43 and gap junction communication in vascular smooth muscle cells of spontaneously hypertensive rats

Wang

Liu

Zhang

et al. 2016

Molecular Medicine Reports

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“…Nevertheless, WNT5A could also regulate a GJIC-independent function of Cx43. In some cells, Cx43 has been linked to intracellular functions that can regulate cell buffering of Ca 2þ , Na 2þ , and ATP independently of its function in intercellular communication [32][33][34][35]. Unknown GJIC-independent pathways could also have effects on myoepithelial cells that could influence contractility or response to oxytocin treatment.…”

Section: Discussionmentioning

confidence: 99%

Misexpression of Wingless-Related MMTV Integration Site 5A in Mouse Mammary Gland Inhibits the Milk Ejection Response and Regulates Connexin43 Phosphorylation1

Baxley

Jiang

Serra

2011

Biology of Reproduction

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Wingless-related MMTV integration site 5A (Wnt5a) is a noncanonical signaling WNT that is expressed in every stage of mouse mammary gland development except lactation. Using slow release pellets containing WNT5A as well as Wnt5a-null tissue, we previously showed that WNT5A acts to limit mammary development. Here, we generated transgenic mice that overexpress WNT5A in the mammary epithelium using the mouse mammary tumor virus promoter (M5a mice). Lactation was impaired in two high WNT5A-expressing lines. Lactation defects could not be explained by differences in apoptosis, lineage differentiation, milk synthesis, or secretion. Instead, misexpression of WNT5A led to a failure in oxytocin response and milk ejection. Noting the similarity between the M5a phenotype and that of mice with a mutation in connexin43 (Cx43; official gene symbol Gja1), we examined Cx43 phosphorylation and localization in M5a mice. In wild-type mice, Cx43 switched from a phosphorylated to a more hypophosphorylated form after parturition. In contrast, the phosphorylated form of Cx43 was maintained after parturition in M5a mice. Using a nontumorigenic breast cell line, MCF10A, we showed that, in addition to increasing the levels of phosphorylation of Cx43 on serine-368, ectopic expression of WNT5A reduced or blocked the amount of dye transferred between cells. In summary, we propose that WNT5A inhibits the response to oxytocin and prevents milk ejection through regulation of Cx43 function.

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“…Cnx43 expressing cells better integrate when applied to the myocardium [40]. Cnx43 also improves cell survival and proliferation [41, 42]. Western blots were performed to assess Cnx43 expression in strained CPCs.…”

Section: Resultsmentioning

confidence: 99%

Fibronectin and Cyclic Strain Improve Cardiac Progenitor Cell Regenerative Potential In Vitro

French

Maxwell

Bhutani

et al. 2016

Stem Cells International

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Cardiac progenitor cells (CPCs) have rapidly advanced to clinical trials, yet little is known regarding their interaction with the microenvironment. Signaling cues present in the microenvironment change with development and disease. This work aims to assess the influence of two distinct signaling moieties on CPCs: cyclic biaxial strain and extracellular matrix. We evaluate four endpoints for improving CPC therapy: paracrine signaling, proliferation, connexin43 expression, and alignment. Vascular endothelial growth factor A (about 900 pg/mL) was secreted by CPCs cultured on fibronectin and collagen I. The application of mechanical strain increased vascular endothelial growth factor A secretion 2–4-fold for CPCs cultured on poly-L-lysine, laminin, or a naturally derived cardiac extracellular matrix. CPC proliferation was at least 25% higher on fibronectin than that on other matrices, especially for lower strain magnitudes. At 5% strain, connexin43 expression was highest on fibronectin. With increasing strain magnitude, connexin43 expression decreased by as much as 60% in CPCs cultured on collagen I and a naturally derived cardiac extracellular matrix. Cyclic mechanical strain induced the strongest CPC alignment when cultured on fibronectin or collagen I. This study demonstrates that culturing CPCs on fibronectin with 5% strain magnitude is optimal for their vascular endothelial growth factor A secretion, proliferation, connexin43 expression, and alignment.

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Connexin 43 hemichannel regulates H9c2 cell proliferation by modulating intracellular ATP and [Ca<sup>2</sup><sup>+</sup>]

Cited by 46 publications

References 63 publications

Enhanced expression of Cx43 and gap junction communication in vascular smooth muscle cells of spontaneously hypertensive rats

Enhanced expression of Cx43 and gap junction communication in vascular smooth muscle cells of spontaneously hypertensive rats

Misexpression of Wingless-Related MMTV Integration Site 5A in Mouse Mammary Gland Inhibits the Milk Ejection Response and Regulates Connexin43 Phosphorylation1

Fibronectin and Cyclic Strain Improve Cardiac Progenitor Cell Regenerative Potential In Vitro

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