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- W2002535159 abstract "Following cardiac injury, activated cardiac myofibroblasts can influence tissue electrophysiology. A popular hypothesis for myofibroblast-induced conduction abnormalities is that myofibroblasts can electrically couple to myocytes, thereby providing an additional load. Although the existence of functional electrical coupling is controversial, the commonly observed close proximity of myofibroblast and myocyte membranes suggests that heterocellular communication could be operating. Based on our preliminary results, we tested the hypothesis that cardiac tissue electrophysiology is affected by mechanical coupling through adherens junctions between myofibroblasts and myocytes. Our recently published data show that after application of the excitation-contraction uncoupler, blebbistatin, or the mechanosensitive channel (MSC) blocker, gadolinium or streptomycin, conduction velocity (CV) was dramatically increased to near control levels in fibrotic monolayers (co-cultured myofibroblasts and neonatal rat ventricular myocytes (NRVMs) treated with transforming growth factor-beta). Using pan-cadherin and N-cadherin antibodies, we also visualized cadherin junctions between myocytes and myofibroblasts. We hypothesized that OB-cadherin is the predominant myofibroblast cadherin in the heterocellular junctions because it is upregulated upon fibroblast activation to myofibroblast and is associated with wound healing. However, CV remained slow upon co-culturing OB-cadherin silenced myofibroblasts with cardiomyocytes, and could still be restored with the addition of MSC and contraction blockers, suggesting that OB-cadherin is not the predominant myofibroblast cadherin in heterocellular junctions. Alternatively, longitudinal and transverse CV in NRVM monolayers supplemented with myofibroblasts and neutralizing N-cadherin antibodies was significantly faster (19.±0.8 cm/s and 6.6±0.3 cm/s, respectively, n=3) than in myofibroblast-supplemented NRVM monolayers lacking such antibodies (10.4±0.9 cm/s and 4.3±0.5cm/s, respectively, n=3, P<0.05). These observations suggest that cardiac conduction can be impaired as a result of coupling of myofibroblasts to myocytes through N-cadherin, which may allow the transmission of tugging forces from the myofibroblasts to activate MSCs." @default.
- W2002535159 created "2016-06-24" @default.
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- W2002535159 date "2012-01-01" @default.
- W2002535159 modified "2023-09-26" @default.
- W2002535159 title "Myofibroblast-Myocyte Coupling Through Adherens Junctions Slows Cardiac Electrical Propagation" @default.
- W2002535159 doi "https://doi.org/10.1016/j.bpj.2011.11.222" @default.
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