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MiR-31 Downregulation Protects Against Cardiac Ischemia/Reperfusion Injury by Targeting Protein Kinase C Epsilon (PKCε) Directly.

AbstractBACKGROUND:
Various miRNAs have been shown to participate in cardiac ischemia/reperfusion injury (I/R). miR-31 was identified as the most strikingly upregulated miRNA after acute myocardial infarction; therefore, the underlying role and mechanism of miR-31 in cardiac I/R was investigated.
METHODS:
miR-31 expression was detected after cardiac I/R in mice. The cardioprotective effect of miR-31 downregulation was assessed in vitro and in vivo. The functional target gene and its downstream molecule were determined.
RESULTS:
miR-31 expression increased after I/R. miR-31 downregulation increased cell viability and SOD activity and decreased LDH activity and MDA content in vitro. Additionally, miR-31 downregulation alleviated myocardial infarct size in vivo. PKCε was identified as the functional target gene of miR-31, and NFκB was identified as its downstream molecule that was involved in the miR-31-mediated cardioprotective effect.
CONCLUSION:
miR-31 expression increased throughout the cardiac I/R process, and miR-31 downregulation induced a cardioprotective effect via a miR-31/PKCε/NFκB-dependent pathway.
AuthorsYongyi Wang, Min Men, Wengang Yang, Hui Zheng, Song Xue
JournalCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology (Cell Physiol Biochem) Vol. 36 Issue 1 Pg. 179-90 ( 2015) ISSN: 1421-9778 [Electronic] Germany
PMID25925791 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • MicroRNAs
  • Mirn31 microRNA, mouse
  • NF-kappa B
  • Lactate Dehydrogenases
  • Superoxide Dismutase
  • Prkce protein, mouse
  • Protein Kinase C-epsilon
Topics
  • Animals
  • Cell Survival
  • Cells, Cultured
  • Disease Models, Animal
  • Down-Regulation
  • Genetic Therapy
  • Lactate Dehydrogenases (metabolism)
  • Mice
  • MicroRNAs (antagonists & inhibitors, genetics, metabolism)
  • Myocardial Ischemia (complications, metabolism, pathology)
  • Myocardial Reperfusion Injury (metabolism, prevention & control)
  • NF-kappa B (metabolism)
  • Protein Kinase C-epsilon (genetics, metabolism)
  • Signal Transduction
  • Superoxide Dismutase (metabolism)

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