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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
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MicroRNA-103/107 Regulate Programmed Necrosis and Myocardial Ischemia/Reperfusion Injury Through Targeting FADD.

Jian-Xun Wang1, Xiao-Jie Zhang1, Qian Li1

  • 1From the Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, China (J.-X.W., K.W., Y.W., S.T., L.-Y.Z., Y.G., Z.-X.Z., J.L., J.-L.W., P.-f.L.); and State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China (X.-J.Z., Q.L., J.-Q.J., C.F.).

Circulation Research
|June 4, 2015
PubMed
Summary

This study reveals a new model for regulating myocardial necrosis involving H19, microRNA-103/107, and FADD. Targeting these molecules may offer novel strategies for preventing heart necrosis.

Keywords:
Fas-associated death domain proteinH19 long noncoding RNAischemia/reperfusion injurymiRNAmyocardial infarctionnecrosisoxidative stress

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cell Biology
  • RNA Biology

Background:

  • Cardiomyocyte death, particularly necrosis, is a key feature of heart disease.
  • Regulated forms of necrosis involve receptor-interacting serine/threonine-protein kinases (RIPK1 and RIPK3) and may be modulated by Fas-associated protein with death domain (FADD).
  • MicroRNAs (miRNAs) and long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cellular processes.

Purpose of the Study:

  • To investigate the roles of microRNA-103/107 and H19 in regulating RIPK1- and RIPK3-dependent necrosis.
  • To determine if these molecules target FADD in cardiomyocyte-derived H9c2 cells and in a myocardial infarction model.
  • To elucidate a novel regulatory pathway for myocardial necrosis.

Main Methods:

  • Utilized H9c2 cells and a mouse ischemia/reperfusion model to study necrosis.
  • Investigated the interaction between FADD, RIPK1, and RIPK3 complexes in H2O2-induced necrosis.
  • Employed techniques to assess miRNA and lncRNA targeting and regulation of FADD expression.
  • Examined the effect of modulating miR-103/107 levels on necrosis.

Main Results:

  • FADD plays a role in H2O2-induced necrosis by affecting RIPK1 and RIPK3 complex formation in H9c2 cells.
  • MicroRNA-103/107 directly target FADD, and their knockdown reduces necrosis in cellular and in vivo models.
  • The miR-103/107-FADD pathway is not involved in tumor necrosis factor-α-induced necrosis.
  • Long noncoding RNA H19 directly binds to miR-103/107, regulating FADD expression and necrosis.

Conclusions:

  • A novel regulatory model for myocardial necrosis involving H19, miR-103/107, and FADD has been identified.
  • This pathway is specific to certain types of necrosis, distinct from TNF-α-induced necrosis.
  • Modulating the levels of H19, miR-103/107, and FADD presents a potential therapeutic strategy for preventing myocardial necrosis.