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Related Experiment Video

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NEDDylation promotes endothelial dysfunction: a role for HDAC2.

Deepesh Pandey1, Daijiro Hori2, Jae Hyung Kim1

  • 1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287-4904, USA.

Journal of Molecular and Cellular Cardiology
|February 7, 2015
PubMed
Summary
This summary is machine-generated.

Inhibition of NEDDylation activating enzyme improves endothelial dysfunction by decreasing Arginase2 via HDAC2. This suggests NEDDylation activating enzyme is a potential therapeutic target for atherosclerosis.

Keywords:
AtherosclerosisEndothelial dysfunctionNEDDylationProtein degradationUbiquitinationVascular endothelium

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Area of Science:

  • Vascular Biology
  • Molecular Mechanisms of Disease
  • Protein Modification

Background:

  • Histone deacetylase 2 (HDAC2) regulates endothelial genes and vascular function.
  • HDAC2 levels decrease with atherogenic stimuli like OxLDL, involving proteasomal degradation.
  • NEDDylation, a post-translational modification, is linked to protein degradation.

Purpose of the Study:

  • To investigate the role of NEDDylation in modulating vascular endothelial function through HDAC2 degradation.
  • To explore NEDDylation activating enzyme as a potential therapeutic target for endothelial dysfunction.

Main Methods:

  • Assessed global protein NEDDylation in human aortic endothelial cells (HAEC) after OxLDL exposure.
  • Utilized NEDDylation activating enzyme inhibitor (MLN4924) in mouse aortic rings and HAEC.
  • Examined HDAC2 and Arginase2 levels, activity, and their interaction with NEDD8 conjugation.

Main Results:

  • OxLDL exposure increased global protein NEDDylation in HAEC.
  • MLN4924 treatment prevented OxLDL-induced endothelial dysfunction and normalized HDAC2 levels.
  • MLN4924 reduced Arginase2 expression and activity, and HDAC2 was identified as a NEDD8 conjugation substrate.

Conclusions:

  • Inhibition of NEDDylation activating enzyme ameliorates endothelial dysfunction by reducing Arginase2 levels in an HDAC2-dependent manner.
  • NEDDylation pathway modulation offers a novel therapeutic strategy for endothelial dysfunction and atherosclerosis.