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Role of P62 Protein in Acute Oxidative Stress‐induced Ventricular Arrhythmias
Author(s) -
Hwang Hyun Seok,
Koh Yeojung,
Rodriguez Jose,
Salazar Gloria
Publication year - 2019
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.2019.33.1_supplement.690.11
Subject(s) - oxidative stress , medicine , cardiology , heart rate , ischemia , myocyte , blood pressure
Chronic ischemia depletes myocardial cells of intracellular defenses from excessive oxidative stress often leads to ventricular arrhythmias. Recently, we reported that autophagy adapter protein, p62 modulate the SR Ca handling in myocytes under chronic myocardial injury. Interestingly, oxidant‐induced beta‐adrenergic signaling involved, it is little known how p62 protein contributes to oxidative stress‐related ventricular arrhythmias in the hearts. Purpose To investigate the role of p62 protein on acute ischemia‐induced arrhythmogenesis in the intact heart. Methods Isolated heart from wild‐type (WT) and p62 knockout (KO) mice (n=8 per group) were used at 10–12 weeks of age. Global ischemia protocol applied in isolated heart preparation. Electrocardiography (ECG) recorded during 15 min steady‐state, 30 min ischemia, and 60 min reperfusion to detect heart rate and arrhythmias (premature ventricular contractions; PVCs). At the end of the experiment, ventricles harvested to measure the expression level of proteins, p62, LC3‐I/LC3‐II, and oxi‐CaMII. Results The heart rate (sinus rate) at baseline was not different between the groups. After 30 min ischemia, sinus rate tends to decrease in only p62 KO hearts during the reperfusion. The incidence of arrhythmias significantly attenuated in the p62 KO heart compared to WT heart during the first 15 min of reperfusion (Premature ventricular contraction, PVC/min; WT, 2.71±1.16* vs. 0.26±0.10,* <0.05 vs. WT, Fig.). The deletion of the p62 gene has a beneficial effect on acute oxidative stress‐induced ventricular arrhythmias in the intact hearts. Discussion Our results suggest that p62 protein involve the oxidative stress‐induced arrhythmogenesis in the hearts, and it may be associated with the intrinsic beta‐adrenergic mechanism. Support or Funding Information Florida State University This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .