Catestatin in defense of oxidative-stress-induced apoptosis: A novel mechanism by activating the beta2 adrenergic receptor and PKB/Akt pathway in ischemic-reperfused myocardium.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Inc Country of Publication: United States NLM ID: 8008690 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-5169 (Electronic) Linking ISSN: 01969781 NLM ISO Abbreviation: Peptides Subsets: MEDLINE
    • Publication Information:
      Publication: New York, NY : Elsevier Science Inc.
      Original Publication: Fayetteville, N. Y., Ankho International.
    • Subject Terms:
      Apoptosis/*drug effects ; Chromogranin A/*pharmacology ; Myocardial Reperfusion Injury/*metabolism ; Myocardium/*metabolism ; Oxidative Stress/*drug effects ; Peptide Fragments/*pharmacology ; Proto-Oncogene Proteins c-akt/*metabolism ; Receptors, Adrenergic, beta-2/*metabolism ; Signal Transduction/*drug effects; Animals ; Male ; Myocardial Reperfusion Injury/drug therapy ; Myocardial Reperfusion Injury/pathology ; Myocardium/pathology ; Rats ; Rats, Sprague-Dawley
    • Abstract:
      Apoptosis induced by oxidative stress is one of the most important cardiomyocytes losses during ischemia-reperfusion (I/R). Catestatin (CST) has been demonstrated to have the anti-oxidative capacity in vitro. We hypothesized that CST intervention could reduce apoptosis of cardiomyocytes induced by oxidative stress in I/R. In Langendorff-perfused rat heart global I/R model, CST was introduced at the reperfusion stage. In comparison to the control group, CST led to preservation on activities of superoxide dismutase and glutathione peroxidase, improvement of hemodynamics, and reduced infarction area in reperfused myocardium. The protection of CST was also shown by less apoptotic cardiomyocytes in TUNEL staining, less caspase-3 activation, and increased phosphorylation of protein kinase B (PKB/Akt) in Western blot. To further demonstrate the benefits of CST and explore the possible underlying mechanism, H 2 O 2 -challenged primary-cultured neonatal rat cardiomyocytes were used to simulate the oxidative-stressed scenario. CST incubation with the H 2 O 2 -challenged cardiomyocytes led to reduction of apoptosis, which was demonstrated by less Hoechst 33342 positive staining of nuclei, less caspase-3 activation, and DNA fragmentation. The effect of CST was abrogated by pretreatment of the cardiomyocytes with the PI3K inhibitor LY294002. Furthermore, Akt activation and the anti-apoptosis effect of CST were abolished by pretreatment of the cardiomyocytes with β2 receptor inhibitor ICI118551. Thus, the salvage of oxidative-stress-induced apoptotic cardiomyocytes in I/R by CST might involve activation β2 receptor and regulation of PI3K/Akt signaling in reperfusion injury salvage kinase (RISK) pathway.
      (Copyright © 2019. Published by Elsevier Inc.)
    • Contributed Indexing:
      Keywords: Apoptosis; Beta2 adrenergic receptor; Catestatin; Ischemia-reperfusion; Oxidative stress
    • Accession Number:
      0 (Adrb2 protein, rat)
      0 (Chromogranin A)
      0 (Peptide Fragments)
      0 (Receptors, Adrenergic, beta-2)
      0 (chromogranin A (344-364))
      EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
    • Publication Date:
      Date Created: 20191116 Date Completed: 20201210 Latest Revision: 20201214
    • Publication Date:
      20240829
    • Accession Number:
      10.1016/j.peptides.2019.170200
    • Accession Number:
      31730792