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Molecular Mechanisms of Electroacupuncture‐Induced Cardioprotection
Author(s) -
Roessler Anne,
Ren Xiaoping,
Luther Kristin,
Jones W Keith
Publication year - 2015
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.29.1_supplement.1025.14
Subject(s) - cardioprotection , medicine , ischemic preconditioning , ischemia , electroacupuncture , heat shock protein , stimulus (psychology) , myocardial infarction , pharmacology , neuroscience , cardiology , chemistry , biology , acupuncture , gene , pathology , psychology , biochemistry , alternative medicine , psychotherapist
A non‐ischemic, nociceptive stimulus such as electroacupunture (EA) in distant tissues can result in the most powerful cardioprotection reported – an 80% decrease in infarct size – called remote preconditioning of trauma (RPCT). It is known that the mechanisms underlying ischemic preconditioning, remote ischemic preconditioning, and RPCT are similar. Whether the downstream genes implicated in other cardioprotective stimuli are also involved in RPCT remains to be determined and is the objective of this study. Specifically, this study will address the hypothesis that electroacupuncture (EA) as a remote nociceptive stimulus is cardioprotective and increases NF‐κB dependent expression of heat shock proteins in the heart. Activation of heat shock proteins (HSPs) by the transcription factor NF‐κB is necessary for late IPC. Preliminary data supports that NF‐κB is required for protection against myocardial infarction 24h after RPCT. qRT‐PCR and Western Blotting were used to assess the changes in gene and protein levels following EA in a mouse model. Previous studies indicate that EA reduces infarct size after occlusion of the left coronary artery. We show that EA of skin results in significant increases in levels of cardiac mRNA levels of HSP90 and DNAJs 3 hours post‐stimulus. Protein accumulation and kinetics are under investigation and confirmatory studies with knockout mice are planned. Future studies will further address the molecular mechanisms of cardioprotection associated with EA therapy. Understanding the mechanism of RPTC via nociception would facilitate the development of non‐invasive therapies, which might be used to precondition patients against ischemia/reperfusion injury by mimicking remote cardioprotection.