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Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning.

Publication ,  Journal Article
Jiang, S; Streeter, J; Schickling, BM; Zimmerman, K; Weiss, RM; Miller, FJ
Published in: Cardiovasc Res
April 1, 2014

AIMS: Ischaemic preconditioning (IPC) is an adaptive mechanism that renders the myocardium resistant to injury from subsequent hypoxia. Although reactive oxygen species (ROS) contribute to both the early and late phases of IPC, their enzymatic source and associated signalling events have not yet been understood completely. Our objective was to investigate the role of the Nox1 NADPH oxidase in cardioprotection provided by IPC. METHODS AND RESULTS: Wild-type (WT) and Nox1-deficient mice were treated with three cycles of brief coronary occlusion and reperfusion, followed by prolonged occlusion either immediately (early IPC) or after 24 h (late IPC). Nox1 deficiency had no impact on the cardioprotection afforded by early IPC. In contrast, deficiency of Nox1 during late IPC resulted in a larger infarct size, cardiac remodelling, and increased myocardial apoptosis compared with WT hearts. Furthermore, expression of Nox1 in WT hearts increased in response to late IPC. Deficiency of Nox1 abrogated late IPC-mediated activation of cardiac nuclear factor-κB (NF-κB) and induction of tumour necrosis factor-α (TNF-α) in the heart and circulation. Finally, knockdown of Nox1 in cultured cardiomyocytes prevented TNF-α induction of NF-κB and the protective effect of IPC on hypoxia-induced apoptosis. CONCLUSIONS: Our data identify a critical role for Nox1 in late IPC and define a previously unrecognized link between TNF-α and NF-κB in mediating tolerance to myocardial injury. These findings have clinical significance considering the emergence of Nox1 inhibitors for the treatment of cardiovascular disease.

Duke Scholars

Published In

Cardiovasc Res

DOI

EISSN

1755-3245

Publication Date

April 1, 2014

Volume

102

Issue

1

Start / End Page

79 / 87

Location

England

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Reactive Oxygen Species
  • NF-kappa B
  • NADPH Oxidase 1
  • NADH, NADPH Oxidoreductases
  • Myocytes, Cardiac
  • Myocardial Reperfusion Injury
  • Myocardial Infarction
  • Mice, Inbred C57BL
  • Male
 

Citation

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Jiang, S., Streeter, J., Schickling, B. M., Zimmerman, K., Weiss, R. M., & Miller, F. J. (2014). Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning. Cardiovasc Res, 102(1), 79–87. https://doi.org/10.1093/cvr/cvu027
Jiang, Shuxia, Jennifer Streeter, Brandon M. Schickling, Kathy Zimmerman, Robert M. Weiss, and Francis J. Miller. “Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning.Cardiovasc Res 102, no. 1 (April 1, 2014): 79–87. https://doi.org/10.1093/cvr/cvu027.
Jiang S, Streeter J, Schickling BM, Zimmerman K, Weiss RM, Miller FJ. Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning. Cardiovasc Res. 2014 Apr 1;102(1):79–87.
Jiang, Shuxia, et al. “Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning.Cardiovasc Res, vol. 102, no. 1, Apr. 2014, pp. 79–87. Pubmed, doi:10.1093/cvr/cvu027.
Jiang S, Streeter J, Schickling BM, Zimmerman K, Weiss RM, Miller FJ. Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning. Cardiovasc Res. 2014 Apr 1;102(1):79–87.
Journal cover image

Published In

Cardiovasc Res

DOI

EISSN

1755-3245

Publication Date

April 1, 2014

Volume

102

Issue

1

Start / End Page

79 / 87

Location

England

Related Subject Headings

  • Tumor Necrosis Factor-alpha
  • Reactive Oxygen Species
  • NF-kappa B
  • NADPH Oxidase 1
  • NADH, NADPH Oxidoreductases
  • Myocytes, Cardiac
  • Myocardial Reperfusion Injury
  • Myocardial Infarction
  • Mice, Inbred C57BL
  • Male