We are analyzing https://link.springer.com/article/10.1007/s00395-016-0577-y.

Title:
Protective role of heme oxygenase-1 in atrial remodeling | Basic Research in Cardiology
Description:
Structural and electrical remodeling in the atrium constitutes the main feature of atrial fibrillation (AF), which is characterized by increased oxidative stress. Heme oxygenase-1 (HO-1) is a potent anti-oxidant system that may provide protection against various oxidative stress-related diseases. The aim of this study is to investigate whether HO-1 has a protective effect on AF-related remodeling. Cultured atrium-derived myocytes (HL-1 cell line) were used to evaluate tachypacing-induced oxidative stress, structural, and electrical remodeling. Transforming growth factor-β (TGF-β) was utilized to assess collagen (a main fibrosis-related protein) expression in atrial fibroblasts. Tachypacing in HL-1 myocytes and treatment of atrial fibroblasts with TGF-β enhanced the expression of HO-1, both of which were mediated by the activation of nuclear factor erythroid-2-related factor 2. Over-expression of HO-1 in HL-1 cells attenuated tachypacing-induced oxidative stress, myofibril degradation, down-regulation of L-type calcium channel, and shortening of action potential duration. Furthermore, HO-1 over-expression in atrial fibroblasts blocked the up-regulation of collagen by TGF-β, implicating a protective role of HO-1 in structural and electrical remodeling in the atrium. In vivo, HO-1−/− mice exhibited a higher degree of oxidative stress, myofibril degradation, and collagen deposit in their atria than wild-type mice. Moreover, burst atrial pacing induced a greater susceptibility to AF in HO-1−/− mice than in wild-type mice. In conclusion, a negative-feedback regulation of HO-1 in activated atrial myocytes and fibroblasts may provide protection against AF-related remodeling and AF development.
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Keywords {🔍}

article, atrial, pubmed, google, scholar, cas, heme, oxygenase, chen, fibrillation, remodeling, chang, cardiol, res, yeh, basic, oxidative, mice, kuo, stress, hsu, myocytes, cardiac, central, dois, circulation, research, cell, expression, access, nadph, lin, gene, author, privacy, cookies, content, protective, role, structural, electrical, fibroblasts, factor, zhang, oxidase, chau, vascular, inhibits, information, publish,

Topics {✒️}

akt/nrf2/heme oxygenase-1 pathway camp-responsive element-binding protein l-type calcium channel oxidative stress-related diseases transforming growth factor-beta main fibrosis-related protein month download article/chapter transforming growth factor-β heme oxygenase-1/carbon monoxide cultured atrial-derived myocytes heme oxygenase-1 gene potent anti-oxidant system der rubart-von lm wei-jan chen cultured atrium-derived myocytes ldl-receptor knockout mice apolipoprotein e-deficient mice article basic research vascular protective factor increased oxidative stress nsc 99-2314-b-182a-050-my2 heme oxygenase-1 expression heme oxygenase-1 protects heme oxygenase-1 genotype high blood pressure chi-tai kuo ying-hwa chen full article pdf oxidative stress human atrial fibrillation chang gung university cultured atrial myocytes cardiac myocyte function privacy choices/manage cookies nadph oxidase signaling activated atrial myocytes curb cardiac pathology lanson na jr hl-1 cell line af-related remodeling proarrhythmic atrial remodeling heme oxygenase-1 izzo nj jr wild-type mice atrial fibrosis article yeh related subjects left atrial myocardium left atrial appendage hsu contribute equally

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         headline:Protective role of heme oxygenase-1 in atrial remodeling
         description:Structural and electrical remodeling in the atrium constitutes the main feature of atrial fibrillation (AF), which is characterized by increased oxidative stress. Heme oxygenase-1 (HO-1) is a potent anti-oxidant system that may provide protection against various oxidative stress-related diseases. The aim of this study is to investigate whether HO-1 has a protective effect on AF-related remodeling. Cultured atrium-derived myocytes (HL-1 cell line) were used to evaluate tachypacing-induced oxidative stress, structural, and electrical remodeling. Transforming growth factor-β (TGF-β) was utilized to assess collagen (a main fibrosis-related protein) expression in atrial fibroblasts. Tachypacing in HL-1 myocytes and treatment of atrial fibroblasts with TGF-β enhanced the expression of HO-1, both of which were mediated by the activation of nuclear factor erythroid-2-related factor 2. Over-expression of HO-1 in HL-1 cells attenuated tachypacing-induced oxidative stress, myofibril degradation, down-regulation of L-type calcium channel, and shortening of action potential duration. Furthermore, HO-1 over-expression in atrial fibroblasts blocked the up-regulation of collagen by TGF-β, implicating a protective role of HO-1 in structural and electrical remodeling in the atrium. In vivo, HO-1−/− mice exhibited a higher degree of oxidative stress, myofibril degradation, and collagen deposit in their atria than wild-type mice. Moreover, burst atrial pacing induced a greater susceptibility to AF in HO-1−/− mice than in wild-type mice. In conclusion, a negative-feedback regulation of HO-1 in activated atrial myocytes and fibroblasts may provide protection against AF-related remodeling and AF development.
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