AI Article Synopsis

  • The study investigates the role of COX-2, an enzyme linked to heart injury and death, in the context of myocardial infarction and its absence in healthy hearts.
  • Researchers created transgenic mice that express human COX-2 in heart cells, finding that these mice showed improved recovery and less cell death during heart ischemia-reperfusion injuries.
  • Proteomic analysis of the mice revealed a significant increase in mitochondrial proteins, particularly in those involved with the respiratory chain, suggesting that COX-2 enhances heart cell energy production and offers protection against injury.

Article Abstract

The biochemical mechanisms of cell injury and myocardial cell death after myocardial infarction remain unresolved. Cyclooxygenase 2 (COX-2), a key enzyme in prostanoid synthesis, is expressed in human ischemic myocardium and dilated cardiomyopathy, but it is absent in healthy hearts. To assess the role of COX-2 in cardiovascular physiopathology, we developed transgenic mice that constitutively express functional human COX-2 in cardiomyocytes under the control of the α-myosin heavy chain promoter. These animals had no apparent phenotype but were protected against ischemia-reperfusion injury in isolated hearts, with enhanced functional recovery and diminished cellular necrosis. To further explore the phenotype of this animal model, we carried out a differential proteome analysis of wild-type vs. transgenic cardiomyocytes. The results revealed a tissue-specific proteomic profile dominated by mitochondrial proteins. In particular, an increased expression of respiratory chain complex IV proteins was observed. This correlated with increased catalytic activity, enhanced respiratory capacity, and increased ATP levels in the heart of COX-2 transgenic mice. These data suggest a new link between COX-2 and mitochondria, which might contribute to the protective cardiac effects of COX-2 against ischemia-reperfusion injury.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9655412PMC
http://dx.doi.org/10.3390/ijms232113476DOI Listing

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