title: NF-κB-mediated induction of autophagy in cardiac ischemia/reperfusion injury.
abstract: Ischemia/reperfusion (I/R) injury severely attenuates the benefit of revascularization after acute myocardial infarction, in which transcription factor NF-κB plays an important role. Recently, there is increasing evidence to suggest that autophagy is involved in this process. We sought to define the role of NF-κB in the induction of autophagy during cardiac I/R injury. The left circumflex coronary arteries of New Zealand white rabbits were ligated for 1.5h, followed by reperfusion for 1h to induce I/R injury. Production of reactive oxygen species (ROS) was detected in myocardial injury area following I/R injury. Furthermore, the results indicated that the cardiac area at risk (AAR) for ischemia has the most abundant expression of Beclin 1 in parallel to p65 expression after cardiac I/R injury. Inhibition of NF-κB significantly attenuated Beclin 1 expression and autophagy in the AAR, which was associated with a marked reduction in the extent of the AAR. Our data thus suggests that I/R injury promotes NF-κB activity, in response to ROS, to aggravate myocardial injury through the activation of Beclin 1-mediated autophagy.
authors.affiliation: The People's Hospital of Hainan Province, Haikou, China. hndzm6@126.com
authors.forename: Min
authors.initials: M
authors.lastname: Zeng
authors.forename: Xin
authors.initials: X
authors.lastname: Wei
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: Wu
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Bing
authors.initials: B
authors.lastname: Li
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhen
authors.forename: Jixiong
authors.initials: J
authors.lastname: Chen
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.forename: Yi
authors.initials: Y
authors.lastname: Fei
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001343:Autophagy / Q000502:physiology*; D015153:Blotting, Western; D003331:Coronary Vessels / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008854:Microscopy, Electron; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D016328:NF-kappa B / Q000378:metabolism / Q000502:physiology*; D011817:Rabbits; D017382:Reactive Oxygen Species / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D051996:Transcription Factor RelA; D008315:Malondialdehyde