title: Loss of plasma membrane integrity, complement response and formation of reactive oxygen species during early myocardial ischemia/reperfusion.
abstract: Loss of plasma membrane integrity (LPMI) is a hallmark of necrotic cell death. The involvement of complement and ROS in the development of LPMI during the early stages of murine myocardial ischemia-reperfusion injury was investigated. LPMI developed within 1 h of reperfusion to a level that was sustained through 24 h. C3 deposition became significant at 3-h reperfusion and thus contributed little to LPMI prior to this time. SOD1 transgenic mice had significantly less LPMI compared with WT mice at 1 h of reperfusion but not at later time points. Catalase transgenic mice were not protected from LPMI at 1-h reperfusion compared with WT mice, but had 69% less LPMI at 3-h reperfusion. This protection was transient. At 24-h reperfusion the LPMI of catalase transgenic mice was identical to that of WT mice. The delayed benefits of over-expressed catalase compared with SOD1 are consistent with its antioxidant action downstream of SOD1. The onset of LPMI occurs within 1 h of reperfusion at a level that is maintained through 24 h. ROS contribute significantly to LPMI during the first 3 h of reperfusion, while complement deposition, which becomes significant after 3-h reperfusion, may contribute thereafter.
authors.affiliation: Department of Anesthesiology, SUNY-Downstate Medical Center, Brooklyn, NY 11203, United States.
authors.forename: Pradeepkumar
authors.initials: P
authors.lastname: Charlagorla
authors.forename: Junying
authors.initials: J
authors.lastname: Liu
authors.forename: Monaliben
authors.initials: M
authors.lastname: Patel
authors.forename: Julie I
authors.initials: JI
authors.lastname: Rushbrook
authors.forename: Ming
authors.initials: M
authors.lastname: Zhang
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002374:Catalase / Q000235:genetics / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism*; D003176:Complement C3 / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D015428:Myocardial Reperfusion Injury / Q000235:genetics / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism*; D013997:Time Factors
chemical_list: D003176:Complement C3; D017382:Reactive Oxygen Species; D002374:Catalase; D013482:Superoxide Dismutase
keywords: Catalase; Complement; Inflammation; Loss of plasma membrane integrity (LPMI); Myocardial ischemia; Necrosis; Reactive oxygen species (ROS); Reperfusion injury; SOD1
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