Abstract
BackgroundTo investigate the effects of semaphorin 3A (sema 3A) on cardiac autonomic regulation and subsequent ventricular arrhythmias (VAs) in post-infarcted hearts.Method and resultsIn order to explore the functions of sema 3A in post-infarcted hearts, lentivirus-Sema 3A-shRNA and negative control vectors were delivered to the peri-infarcted myocardium rats respectively. Meanwhile, recombinant sema 3A and control (0.9 % NaCl solution) were injected intravenously into infarcted rats to test the therapeutic potential of sema 3A. Results indicated that levels of sema 3A were higher in post-infarcted hearts compared with sham rats. However, sema 3A silencing leaded to sympathetic hyperinnervation, increased myocardial norepinephrine (NE) content and inducible VAs. Conversely, the intravenous administration of sema 3A to infarcted rats reduced sympathetic nerve sprouting, improved cardiac autonomic regulation, and decreased the incidence of inducible VAs. However, both infarct size and cardiac function were similar among infarcted hearts.ConclusionsThe upregulation and administration of sema 3A exerted beneficial effects on infarction-induced cardiac autonomic disorders by increasing cardiac electrical stability and reducing VAs. Sema 3A might be a potential therapeutic agent for cardiac autonomic abnormalities induced arrhythmias.
Highlights
To investigate the effects of semaphorin Semaphorin 3A (3A) on cardiac autonomic regulation and subsequent ventricular arrhythmias (VAs) in post-infarcted hearts
Preparation of semaphorin 3A (sema 3A) short hairpin RNA (shRNA) lentiviral vector RNA interference (RNAi) is a post-transcriptional process that is triggered by the introduction of double-stranded RNA, which leads to gene silencing in a sequence-specific manner
Compared with the MIGFP group, the expression of sema 3A was significantly lower in the myocardial infarction (MI)-SiRNA group (P < 0.01, Fig. 2)
Summary
To investigate the effects of semaphorin 3A (sema 3A) on cardiac autonomic regulation and subsequent ventricular arrhythmias (VAs) in post-infarcted hearts. Despite advances in management strategies and patient education, ventricular arrhythmias (VAs) remain an unsolved problem, and the identification for patients at a high risk of sudden cardiac death due to myocardial infarction (MI) is still challenging [1, 2]. Neural control of the heart is mediated through the parasympathetic and sympathetic branches of the autonomic nervous system, which jointly maintain the normal cardiac function and electrophysiological stability via innervation balance. MI induces nerve reinnervations including sympathetic nerve and cholinergic nerve fibers [11], and infarctioninduced nerve sprouting is mainly sympathetic nerve. Infarction-induced cardiac autonomic abnormalities might lead to sympathetic overactivation and subsequent VAs
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