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The p65 subunit of NF-κB involves in RIP140-mediated inflammatory and metabolic dysregulation in cardiomyocytes

Luankun Zhang1, Yanfang Chen2, Zhongbao Yue1

  • 1Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, PR China.

Archives of Biochemistry and Biophysics
|May 15, 2014
PubMed

Insights

The transcription factor NF-κB is crucial for RIP140

Area of Science:

  • Cardiovascular Biology
  • Molecular Metabolism
  • Inflammation Research

Background:

  • Nuclear factor kappa B (NF-κB) regulates genes in inflammation and metabolism, impacting cardiac pathology.
  • RIP140 is a corepressor inhibiting genes for substrate uptake and mitochondrial beta-oxidation, and can coactivate p65-NF-κB in macrophages.

Purpose of the Study:

  • To investigate the role of RIP140 in cardiomyocytes.
  • To elucidate the interplay between RIP140, p65-NF-κB, and cardiac inflammation and metabolism.

Main Methods:

  • Overexpression of RIP140 in neonatal rat cardiomyocytes.
  • Inhibition of p65-NF-κB.
  • Knockdown of p65-NF-κB.
  • Analysis of proinflammatory gene expression and cytokine release.
  • Assessment of metabolic-related genes, mitochondrial biogenesis, and metabolic function.

Main Results:

  • RIP140 overexpression induced proinflammatory gene expression and cytokine release in cardiomyocytes.
  • These RIP140 effects were reversed by p65-NF-κB inhibition.
  • RIP140's repression of metabolic genes and mitochondrial function was attenuated by p65-NF-κB knockdown.

Conclusions:

  • p65-NF-κB is integral to RIP140-induced inflammation and metabolic alterations in cardiomyocytes.
  • This study highlights the crosstalk between cardiac inflammation and metabolic dysfunction.
Keywords:
Cardiac energy metabolismInflammationMitochondriaNF-κBRIP140

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