Correlation Engine 2.0
Clear Search sequence regions

  • apoptosis (7)
  • base sequence (1)
  • cardiovascular diseases (1)
  • cells (1)
  • gene (2)
  • heart (1)
  • heart diseases (1)
  • ischemia (1)
  • ischemia- cardiac (1)
  • mice (1)
  • micrornas (4)
  • miR 22 (8)
  • MIRN22 (1)
  • mitogen (2)
  • myocardium (1)
  • newborn (1)
  • p38 (2)
  • p38α (3)
  • pcr (1)
  • protein kinases (2)
  • rat (5)
  • regulates (1)
  • rnas (2)
  • tunel (1)
  • western blot (1)
  • Sizes of these terms reflect their relevance to your search.

    microRNAs (miRNAs) are short noncoding RNAs that function in RNA silencing and post-transcriptional regulation of gene expression. They play critical regulatory roles in many cardiovascular diseases, including ischemia-induced cardiac injury. Here, we report microRNA-22, highly expressed in the heart, can protect cardiomyocytes from starvation-induced injury through promoting autophagy and inhibiting apoptosis. Quantitative real-time PCR (qPCR) demonstrated that the expression of miR-22 in starvation-treated neonatal rat cardiomyocytes (NRCMs) was markedly down-regulated. Over-expression of miR-22 significantly promoted starvation-induced autophagy and inhibited starvation-induced apoptosis in NRCMs. In contrast, reduction of miR-22 suppressed autophagy and accelerated apoptosis in starving NRCMs. Immunohistochemistry and TUNEL staining results also provided further evidence that miR-22 promoted autophagy and inhibited apoptosis in myocardial cells. Furthermore, both luciferase reporter assay and western blot analysis were performed to identify p38α as a direct target of miR-22. Taken together, miR-22 plays an important role in regulating autophagy and apoptosis in ischemic myocardium through targeting p38α. miR-22 may represent a potential therapeutic target for the treatment of ischemic heart diseases. Copyright © 2016 Elsevier Inc. All rights reserved.


    Guoran Li, Guokun Wang, Liangliang Ma, Jun Guo, Jingwen Song, Liping Ma, Xianxian Zhao. miR-22 regulates starvation-induced autophagy and apoptosis in cardiomyocytes by targeting p38α. Biochemical and biophysical research communications. 2016 Sep 23;478(3):1165-72

    Expand section icon Mesh Tags

    Expand section icon Substances

    PMID: 27544030

    View Full Text