title: Semaphorin 3A deficiency improves hypoxia-induced myocardial injury via resisting inflammation and cardiomyocytes apoptosis.
abstract: Ischemia/hypoxia leads to heart injuries by inducing inflammation, cardiac fibrosis and cardiomyocyte apoptosis. Semaphorin 3A (Sema 3A) plays a regulatory role during all immune response stages, and has been demonstrated to be associated with multiple diseases. However, roles of Sema 3A during myocardial ischemia/hypoxia have not been studied in full. In this study, decline in Sema 3A was discovered in hypoxia-treated myocardial cells. When this decline was enhanced by silencing of Sema 3A gene, hypoxia-induced myocardial cell injury could be partially improved. Sema 3A deficiency can resist hypoxia-induced inflammatory factors (TNF-α, IL-1β and IL-6) secretion, cell viability decline, cardiomyocyte apoptosis, ROS release, ATP generation decline as well as GSH/GSSG ratio decline in H9C2 cells. Besides, hypoxia-induced bcl-2 decrease and cleaved caspase-3 increase also can be partially reversed during Sema 3A deficiency. All these findings reflect that reduced Sema 3A is a protective strategy adopted by damaged myocardial cell. Our study first shows that Sema 3A deficiency can improve hypoxia-induced myocardial cell injury, which thus offers a new insight to treatment ischemic heart disease.
authors.affiliation: Tianjin Union Medicine Center Department of Cardiology Tianjin China.
authors.forename: C
authors.initials: C
authors.lastname: Zhao
authors.affiliation: The Fourth Military Medical University Department of Geriatrics, Tangdu Hospital Xi'an China.
authors.forename: J
authors.initials: J
authors.lastname: Liu
authors.affiliation: Tianjin Union Medicine Center Department of Nephrology Tianjin China.
authors.forename: M
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Tianjin Union Medicine Center Department of Nephrology Tianjin China yiqing_wu66@163.com.
authors.forename: Y
authors.initials: Y
authors.lastname: Wu
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D015687:Cell Hypoxia; D002460:Cell Line; D005978:Glutathione / Q000378:metabolism; D007249:Inflammation / Q000235:genetics; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D040121:Semaphorin-3A / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species; D040121:Semaphorin-3A; D014409:Tumor Necrosis Factor-alpha; D000255:Adenosine Triphosphate; D053148:Caspase 3; D005978:Glutathione