title: Ischemia triggered ATP release through Pannexin-1 channel by myocardial cells activates sympathetic fibers.
abstract: The cardiovascular system is extensively innervated by the autonomic nervous system, and the autonomic modulation including sympathetic innervation is crucial to the function of heart during normal and ischemic conditions. Severe myocardial ischemia could cause acute myocardial infarction, which is one of the leading diseases in the world. Thus studying the sympathetic modulation during ischemia could reduce the probability of myocardial infarction and further heart failure. The neurotransmitter ATP is released by myocardial cells during ischemia; however, the effect of ATP release remains elusive. We examined whether ATP released during ischemia functions as a neurotransmitter that activates sympathetic nerve in the heart. A novel technique of recording the sympathetic fiber calcium imaging in mouse cardiac tissue slices was used. We have applied the Cre/loxP system to specifically express GCaMP3, a genetically encoded calcium indicator, in the sympathetic nerve. Using this technique, we found that ATP released by myocardial cells through Pannexin-1 channel during ischemia could evoke calcium responses in cardiac sympathetic nerve fibers. Our study provides a new approach to study the cell and nerve interaction in the cardiac system, as well as a new understanding of ATP function during ischemia.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Suzhou University, Suzhou 215006, Jiangsu, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Dong
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Suzhou University, Suzhou 215006, Jiangsu, China. Electronic address: yangxiangjun@163.com.
authors.forename: Xiang-Jun
authors.initials: XJ
authors.lastname: Yang
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Suzhou University, Suzhou 215006, Jiangsu, China.
authors.forename: Ting-Bo
authors.initials: TB
authors.lastname: Jiang
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Suzhou University, Suzhou 215006, Jiangsu, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000320:Adrenergic Fibers / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects; D002229:Carbenoxolone / Q000494:pharmacology; D017630:Connexins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D007202:Indicators and Reagents / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D017202:Myocardial Ischemia / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D012849:Sinoatrial Node / Q000378:metabolism
chemical_list: D017630:Connexins; D007202:Indicators and Reagents; D009419:Nerve Tissue Proteins; C503631:Panx1 protein, mouse; D011993:Recombinant Fusion Proteins; D000255:Adenosine Triphosphate; D002229:Carbenoxolone; D002118:Calcium
keywords: ATP; GCaMP3; Ischemia; Sympathetic nerve