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The role of microRNA‐21 in anesthetic‐mediated cardioprotection (1155.9)
Author(s) -
Olson Jessica,
Yan Yasheng,
Twaroski Danielle,
Canfield Scott,
Kikuchi Chika,
Kriegel Alison,
Bai Xiaowen,
Liang Mingyu,
Bosnjak Z.
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1155.9
Subject(s) - cardioprotection , microrna , isoflurane , anesthetic , medicine , ischemic preconditioning , downregulation and upregulation , reperfusion injury , induced pluripotent stem cell , ischemia , pharmacology , bioinformatics , biology , anesthesia , embryonic stem cell , gene , biochemistry
In this study, we investigate the role of microRNA‐21 in anesthetic preconditioning, and its disruption in diabetic models. Anesthetic‐mediated cardioprotection has been shown to decrease myocardial infarct size after ischemia‐reperfusion injury. This response is drastically attenuated in diabetic patients. Many cell signaling pathways have been investigated in this phenomenon; however, the role of microRNA remains unknown. MicroRNAs are short, non‐coding nucleotide sequences that negatively regulate gene expression through degradation or suppression of messenger RNA. Using qRT‐PCR, our lab has shown a continuous upregulation in microRNA‐21 after isoflurane exposure that appears to play an important role in cardioprotection through its actions on programmed cell death protein 4. This powerful protective cell signaling pathway is disrupted in multiple models of diabetes, including induced pluripotent stem cell‐derived cardiomyocytes from patients with type 2 diabetes, and in patient‐derived cardiomyocytes exposed to high glucose. Our data indicate an important role of microRNA‐21 in isoflurane‐induced cardioprotection and the impairment of this pathway by diabetic conditions. Further investigation may suggest new therapeutic targets for reducing cardiovascular morbidity and mortality in high‐risk patients. Grant Funding Source : Supported by NIH Grants RO1HL034708 and P01GM06673 for Zeljko J. Bosnjak.