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Poster Session 4Session Title: Myocardial Ischemia and Cardioprotection

Abstract P276: Cardiac-Specific Knockout NF-kB Mice Resist Dysfunction Induced by Global Ischemia-Reperfusion

Xiu Q Zhang, Ling Li, Yubin Deng, Lensey Scott, Craig Selzman
Circulation Research. 2011;109:AP276
Xiu Q Zhang
Univ of Utah, Salt Lake City, UT
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Ling Li
Univ of Utah, Salt Lake City, UT
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Yubin Deng
Univ of Utah, Salt Lake City, UT
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Lensey Scott
Univ of Utah, Salt Lake City, UT
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Craig Selzman
Univ of Utah, Salt Lake City, UT
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Abstract

Subjective: Nuclear factor Kappa B (NF-kB) is a pluripotent transcriptional factor that has been implicated as mediator of cardiac injury after ischemia-reperfusion (IR). Multiple approaches have been used to target inhibition of NF-kB, yet these strategies are often non-specific. P65-NF-kB exists as a heterodimer with its p50 subunit and is the dominant transcriptional subunit of NF-kB. In order to better understand its role in the heart, we have recently generated mice that have cardiomyocyte (CMC) specific deletion of p65 NF-kB and hypothesized that these animals would be protected from ischemic stress.

Methods: Transgenic mice were generated with (WT) or without CMC p65 (KO). NF-kB p65 expression was assessed with Western Blots. We subjected the mice to global IR using Langendorf system with baseline 20 min, ischemia 45 min and reperfusion 60 min. Cardiac contractile functional recovery was analyzed using rate pressure product (RPP), contractility (+dp/dt), and relaxation (-dp/dt). Infarct size was assessed with TTC staining. LDH and CK were measured in reperfused solutions.

Results: 1. No differences were found between groups of WT (n=7) and KO (n=8) in body weight and heart weight. 2. KO mice express significant less cardiac-specific NF-kB p65. 3. During reperfusion, RPP, +dp/dt, -dp/dt recovery to base line were all better in p65 KO mice (RPP: 0.841±0.074 in KO vs 0.635±0.080 in WT; +dp/dt: 0.997±0.096 in KO vs 0.731±0.108 in WT; -dp/dt: 0.869±0.096 in KO vs 0.630±0.090 in WT; p<0.05 respectively). 4. After ischemia, both LDH and CK release were markedly less in solutions collected from p65 KO heart (LDH: 45.2±28.0 u/L; CK: 28.1±23.6 u/L) than those in p65 WT heart (LDH: 143.2±25.9 u/L; CK: 107.2±26.2 u/L; p,0.01 respectively). 5. TTC staining shown significant less necrotic tissue in KO heart vs WT heart (0.314±0.052 vs 0.653±0.061, p<0.05).

Conclusion: CMC-specific knockout NF-kB p65 mice have improved cardiac recovery function, less heart necrosis, and decreased CMC injury compared to WT after global heart ischemia. These studies confirm many of the previous studies suggesting a protective role for anti-NF-kB strategies for ischemia. It furthermore provides a template to further define the mechanisms of p65-NF-kB afforded cardioprotection.

  • Ischemia reperfusion
  • Cardioprotection
  • Transgenic models
  • © 2011 by American Heart Association, Inc.
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Circulation Research
9 December 2011, Volume 109, Issue Suppl 1
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    Abstract P276: Cardiac-Specific Knockout NF-kB Mice Resist Dysfunction Induced by Global Ischemia-Reperfusion
    Xiu Q Zhang, Ling Li, Yubin Deng, Lensey Scott and Craig Selzman
    Circulation Research. 2011;109:AP276, originally published October 8, 2015

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    Abstract P276: Cardiac-Specific Knockout NF-kB Mice Resist Dysfunction Induced by Global Ischemia-Reperfusion
    Xiu Q Zhang, Ling Li, Yubin Deng, Lensey Scott and Craig Selzman
    Circulation Research. 2011;109:AP276, originally published October 8, 2015
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