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Melatonin facilitates adipose-derived mesenchymal stem cells to repair the murine infarcted heart via the SIRT1 signaling pathway.

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  • معلومة اضافية
    • المصدر:
      Publisher: Wiley Country of Publication: England NLM ID: 8504412 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1600-079X (Electronic) Linking ISSN: 07423098 NLM ISO Abbreviation: J Pineal Res Subsets: MEDLINE
    • بيانات النشر:
      Publication: : Oxford : Wiley
      Original Publication: New York : Liss, c1984-
    • الموضوع:
      Mesenchymal Stem Cell Transplantation* ; Signal Transduction*; Adipose Tissue/*metabolism ; Melatonin/*pharmacology ; Mesenchymal Stem Cells/*metabolism ; Myocardial Infarction/*therapy ; Sirtuin 1/*metabolism; Animals ; Female ; Mice ; Mice, Transgenic ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardium/metabolism ; Myocardium/pathology
    • نبذة مختصرة :
      Mesenchymal stem cells (MSCs)-based therapy provides a promising therapy for the ischemic heart disease (IHD). However, engrafted MSCs are subjected to acute cell death in the ischemic microenvironment, characterized by excessive inflammation and oxidative stress in the host's infarcted myocardium. Melatonin, an indole, which is produced by many organs including pineal gland, has been shown to protect bone marrow MSCs against apoptosis although the mechanism of action remains elusive. Using a murine model of myocardial infarction (MI), this study was designed to evaluate the impact of melatonin on adipose-derived mesenchymal stem cells (AD-MSCs)-based therapy for MI and the underlying mechanism involved with a focus on silent information regulator 1(SIRT1) signaling. Our results demonstrated that melatonin promoted functional survival of AD-MSCs in infarcted heart and provoked a synergetic effect with AD-MSCs to restore heart function. This in vivo effect of melatonin was associated with alleviated inflammation, apoptosis, and oxidative stress in infarcted heart. In vitro studies revealed that melatonin exert cytoprotective effects on AD-MSCs against hypoxia/serum deprivation (H/SD) injury via attenuating inflammation, apoptosis, and oxidative stress. Mechanistically, melatonin enhanced SIRT1 signaling, which was accompanied with the increased expression of anti-apoptotic protein Bcl2, and decreased the expression of Ac-FoxO1, Ac-p53, Ac-NF-ΚB, and Bax. Taken together, our findings indicated that melatonin facilitated AD-MSCs-based therapy in MI, possibly through promoting survival of AD-MSCs via SIRT1 signaling. Our data support the promise of melatonin as a novel strategy to improve MSC-based therapy for IHD, possibly through SIRT1 signaling evocation.
      (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
    • Contributed Indexing:
      Keywords: SIRT1 signaling; melatonin; myocardial infarction; oxidative stress; stem cells
    • الرقم المعرف:
      EC 3.5.1.- (Sirt1 protein, mouse)
      EC 3.5.1.- (Sirtuin 1)
      JL5DK93RCL (Melatonin)
    • الموضوع:
      Date Created: 20151127 Date Completed: 20161024 Latest Revision: 20220318
    • الموضوع:
      20221213
    • الرقم المعرف:
      10.1111/jpi.12299
    • الرقم المعرف:
      26607398