1. Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.
- Author
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Nicholas Chun, Ala S Haddadin, Junying Liu, Yunfang Hou, Karen A Wong, Daniel Lee, Julie I Rushbrook, Karan Gulaya, Roberta Hines, Tamika Hollis, Beatriz Nistal Nuno, Abeel A Mangi, Sabet Hashim, Marcela Pekna, Amy Catalfamo, Hsiao-Ying Chin, Foramben Patel, Sravani Rayala, Ketan Shevde, Peter S Heeger, and Ming Zhang
- Subjects
Medicine ,Science - Abstract
The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT C57BL/6 mice, a manipulation that resulted in marked myocardial necrosis associated with activation of fB protein and myocardial deposition of C3 activation products. In contrast, in fB-/- mice, the same procedure resulted in significantly reduced myocardial necrosis (% ventricular tissue necrotic; fB-/- mice, 20 ± 4%; WT mice, 45 ± 3%; P < 0.05) and diminished deposition of C3 activation products in the myocardial tissue (fB-/- mice, 0 ± 0%; WT mice, 31 ± 6%; P
- Published
- 2017
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