A Novel Role of MicroRNA in Late Preconditioning: Upregulation of Endothelial Nitric Oxide Synthase and Heat Shock Protein 70

@article{Yin2009ANR,
  title={A Novel Role of MicroRNA in Late Preconditioning: Upregulation of Endothelial Nitric Oxide Synthase and Heat Shock Protein 70},
  author={Chang Yin and Fadi N. Salloum and Rakesh C. Kukreja},
  journal={Circulation Research},
  year={2009},
  volume={104},
  pages={572-575}
}
MicroRNAs (miRNAs) are noncoding RNAs of 18 to 24 nucleotides that are involved in posttranscriptional regulation of protein expression. Their role in ischemic preconditioning (IPC) is currently unknown. We hypothesized that miRNAs induced after IPC in the heart may create a preconditioned phenotype through upregulating proteins including endothelial nitric oxide synthase (eNOS)/inducible nitric oxide synthase (iNOS) and heat shock protein (HSP)70, which are implicated in the late-phase… 

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References

SHOWING 1-10 OF 21 REFERENCES
The late phase of ischemic preconditioning is abrogated by targeted disruption of the inducible NO synthase gene.
  • Y. Guo, W. Jones, R. Bolli
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1999
TLDR
The results demonstrate that (i) the late phase of ischemic PC is associated with selective up-regulation of iNOS, and (ii) targeted disruption of the iN OS gene completely abrogates the infarct-sparing effect of late PC (but not of early PC), providing unequivocal molecular genetic evidence for an obligatory role ofiNOS in the cardioprotection afforded by the latephase of isChemic PC.
MicroRNAs Play an Essential Role in the Development of Cardiac Hypertrophy
TLDR
It is proposed that microRNAs play an essential regulatory role in the development of cardiac hypertrophy, wherein downregulation of miR-1 is necessary for the relief of growth-related target genes from its repressive influence and induction ofhypertrophy.
Regulation of endothelial nitric oxide synthase by small RNA.
TLDR
It is demonstrated that intron-based microRNAs in eNOS can induce significant gene specific transcriptional suppression, which could be an effective negative feedback regulator for gene expression.
Reactive oxygen species play an important role in the activation of heat shock factor 1 in ischemic-reperfused heart.
TLDR
It is demonstrated that ROSs play an important role in the activation of HSF1 and the accumulation of mRNA for HSP70 and HSP90 in the ischemic-reperfused heart.
Hypoxia Inducible Factor-1 Activation by Prolyl 4-Hydroxylase-2 Gene Silencing Attenuates Myocardial Ischemia Reperfusion Injury
TLDR
In vitro and in vivo, PHD2 silencing using a siRNA strategy produces transcriptionally active HIF-1, which attenuates reperfusion injury via an iNOS-dependent pathway and stabilization in normoxia murine microvascular endothelial cells.
Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis
TLDR
It is found that the miR-1 genes are direct transcriptional targets of muscle differentiation regulators including serum response factor, MyoD and Mef2, and a new algorithm for microRNA target identification that incorporates features of RNA structure and target accessibility is used.
The Late Phase of Preconditioning
TLDR
The cardioprotective effects of late PC can be reproduced pharmacologically with clinically relevant agents (eg, NO donors, adenosine receptors agonists, endotoxin derivatives, or opioid receptor agonists), suggesting that this phenomenon might be exploited for therapeutic purposes.
Cardioprotection: nitric oxide, protein kinases, and mitochondria.
TLDR
The cumulative effect of stunning is a progression to hibernation, and repetitive cycles of ischemia/reperfusion with subsequent stunning finally result in hibernating myocardium with reduced contractile function and baseline blood flow.
...
...