Cardiac proteomics reveals the potential mechanism of microtubule associated protein 4 phosphorylation-induced

Lingfei Li1, Junhui Zhang1, Qiong Zhang1

  • 11Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University (Army Medical University), Gaotanyan Street, Shapingba District, Chongqing, 400038 China.

Burns & Trauma
|March 26, 2019
PubMed
Abstract

Insights

Microtubule associated protein 4 (MAP4) phosphorylation causes mitochondrial dysfunction in cardiomyopathy. This study identified differentially expressed proteins (DEPs) in mouse heart tissue, revealing potential mechanisms linking MAP4 phosphorylation to heart dysfunction.

Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Proteomics

Background:

  • Previous studies linked microtubule associated protein 4 (MAP4) phosphorylation to mitochondrial dysfunction in cardiomyopathy.
  • The precise molecular mechanisms underlying this association remained unclear.

Purpose of the Study:

  • To investigate the detailed mechanism of MAP4 phosphorylation-induced mitochondrial dysfunction in cardiomyopathy.
  • To identify key proteins involved in this process.

Main Methods:

  • Generated a mouse model with constant MAP4 phosphorylation (S737 and S760).
  • Utilized isobaric tag for relative and absolute quantitation (iTRAQ) on heart tissue.
  • Performed Gene Ontology (GO), KEGG pathway, and protein-protein interaction (PPI) analyses on differential expressed proteins (DEPs).

Main Results:

  • Identified 72 cardiac DEPs, with 12 upregulated and 60 downregulated.
  • GO and KEGG analyses revealed affected biological processes, molecular functions, cellular components, and biochemical pathways.
  • Highlighted three key proteins potentially involved in MAP4 phosphorylation-induced mitochondrial dysfunction, validated by Western blot.

Conclusions:

  • MAP4 phosphorylation leads to significant changes in cardiac protein expression.
  • These identified DEPs provide crucial insights into the mechanisms of MAP4 phosphorylation-induced mitochondrial dysfunction and cardiomyopathy.

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