| TNFalpha-initiated oxidative/nitrative stress mediates cardiomyocyte apoptosis in traumatic animals. | |
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MedLine Citation:
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PMID: 17701456 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Whole body non-penetrating trauma causes myocardial infarction in humans and mechanical trauma (MT) results in cardiac dysfunction in animals. Our recent study demonstrated that incubation of cardiomyocytes with plasma isolated from MT animals causes significant cardiomyocyte apoptosis that can be blocked by neutralization of TNFalpha. The present study attempted to obtain direct in vivo evidence to support that overproduction of TNFalpha plays a causative role in trauma-induced cardiomyocyte apoptosis. Non-lethal MT caused significant TNFalpha overproduction (2.4-fold at 1.5 h after MT) and increased cardiomyocyte apoptosis (starting 3 h and peaking 12 h after MT). Pharmacological inhibition of TNFalpha with etanercept or TNFalpha gene deletion reduced post-trauma myocyte apoptosis (P<0.01). Expression of iNOS and NADPH oxidase, overproduction of NO and O2-, and excessive protein nitration in the MT heart were all significantly reduced in etanercept-treated or TNFalpha-/- mice, suggesting that oxidative/nitrative stress may contribute to TNFalpha-initiated myocyte apoptosis in MT hearts. Additional experiments demonstrated that inhibiting iNOS (1400W) or NADPH oxidase (apocynin), or scavenging peroxynitrite (FP15) significantly reduced myocyte apoptosis in MT animals (P<0.01). Collectively, these data demonstrated that non-lethal mechanical trauma caused significant TNFalpha production that in turn stimulated myocardial apoptosis via oxidative/nitrative stress. |
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Authors:
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Shuzhuang Li; Ling Tao; Xiangying Jiao; Huirong Liu; Yue Cao; Bernard Lopez; Rong-Hua Luan; Theodore Christopher; Xin L Ma |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Apoptosis : an international journal on programmed cell death Volume: 12 ISSN: 1360-8185 ISO Abbreviation: Apoptosis Publication Date: 2007 Oct |
Date Detail:
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Created Date: 2007-10-01 Completed Date: 2008-03-27 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9712129 Medline TA: Apoptosis Country: United States |
Other Details:
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Languages: eng Pagination: 1795-802 Citation Subset: IM |
Affiliation:
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Departments of Physiology and Cardiology, Xi-Jing Hospital, The Fourth Military Medical University, Xian, 710032, P.R. China. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetophenones
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metabolism Animals Apoptosis / physiology* Enzyme Inhibitors / metabolism Humans Male Metalloporphyrins / metabolism Mice Mice, Inbred C57BL Mice, Knockout Myocytes, Cardiac / cytology, physiology* Nitric Oxide Synthase Type II / antagonists & inhibitors, metabolism Nitrites / metabolism* Oxidative Stress* Peroxynitrous Acid / metabolism Reactive Nitrogen Species / metabolism Reactive Oxygen Species / metabolism Tumor Necrosis Factor-alpha / genetics, metabolism* Wounds and Injuries* / pathology, physiopathology |
| Grant Support | |
ID/Acronym/Agency:
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2R01HL-63828/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acetophenones; 0/Enzyme Inhibitors; 0/FeCl tetrakis-2-(triethyleneglycolmonomethylether)pyridylporphyrin; 0/Metalloporphyrins; 0/Nitrites; 0/Reactive Nitrogen Species; 0/Reactive Oxygen Species; 0/Tumor Necrosis Factor-alpha; 14691-52-2/Peroxynitrous Acid; 498-02-2/acetovanillone; EC 1.14.13.39/Nitric Oxide Synthase Type II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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