NF-κB-mediated induction of autophagy in cardiac ischemia/reperfusion injury

被引:130
作者
Zeng, Min [1 ]
Wei, Xin [1 ]
Wu, Zhiyong [1 ]
Li, Wei [1 ]
Li, Bing [1 ]
Zhen, Ying [1 ]
Chen, Jixiong [1 ]
Wang, Ping [1 ]
Fei, Yi [1 ]
机构
[1] Peoples Hosp Hainan Prov, Haikou 570311, Peoples R China
关键词
Ischemia/reperfusion; NF-kappa B; Autophagy; ISCHAEMIA/REPERFUSION INJURY; CELL-DEATH; HEART; REPERFUSION; INHIBITION; ACTIVATION; BECLIN-1;
D O I
10.1016/j.bbrc.2013.05.070
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Ischemia/reperfusion (I/R) injury severely attenuates the benefit of revascularization after acute myocardial infarction, in which transcription factor NF-kappa B 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-kappa B in the induction of autophagy during cardiac I/R injury. The left circumflex coronary arteries of New Zealand white rabbits were ligated for 1.5 h, followed by reperfusion for I h 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-kappa B 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-kappa B activity, in response to ROS, to aggravate myocardial injury through the activation of Beclin 1-mediated autophagy. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:180 / 185
页数:6
相关论文
共 23 条
[1]
Inhibition of macroautophagy triggers apoptosis [J].
Boya, P ;
González-Polo, RA ;
Casares, N ;
Perfettini, JL ;
Dessen, P ;
Larochette, N ;
Métivier, D ;
Meley, D ;
Souquere, S ;
Yoshimori, T ;
Pierron, G ;
Codogno, P ;
Kroemer, G .
MOLECULAR AND CELLULAR BIOLOGY, 2005, 25 (03) :1025-1040
[2]
p65/RelA binds and activates the beclin 1 promoter [J].
Copetti, Tamara ;
Demarchi, Francesca ;
Schneider, Claudio .
AUTOPHAGY, 2009, 5 (06) :858-859
[3]
p65/RelA Modulates BECN1 Transcription and Autophagy [J].
Copetti, Tamara ;
Bertoli, Cosetta ;
Dalla, Emiliano ;
Demarchi, Francesca ;
Schneider, Claudio .
MOLECULAR AND CELLULAR BIOLOGY, 2009, 29 (10) :2594-2608
[4]
The IKK complex contributes to the induction of autophagy [J].
Criollo, Alfredo ;
Senovilla, Laura ;
Authier, Helene ;
Maiuri, Maria Chiara ;
Morselli, Eugenia ;
Vitale, Ilio ;
Kepp, Oliver ;
Tasdemir, Ezgi ;
Galluzzi, Lorenzo ;
Shen, Shensi ;
Tailler, Maximilien ;
Delahaye, Nicolas ;
Tesniere, Antoine ;
De Stefano, Daniela ;
Ben Younes, Amena ;
Harper, Francis ;
Pierron, Gerard ;
Lavandero, Sergio ;
Zitvogel, Laurence ;
Israel, Alain ;
Baud, Veronique ;
Kroemer, Guido .
EMBO JOURNAL, 2010, 29 (03) :619-631
[5]
DECKER RS, 1980, AM J PATHOL, V98, P425
[6]
NF-κB activation represses tumor necrosis factor-α-induced autophagy [J].
Djavaheri-Mergny, Mojgan ;
Amelotti, Manuela ;
Mathieu, Julie ;
Besancon, Francoise ;
Bauvy, Chantal ;
Souquere, Sylvie ;
Pierron, Gerard ;
Codogno, Patrice .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (41) :30373-30382
[7]
NF-κB inhibition sensitizes to starvation-induced cell death in high-risk myelodysplastic syndrome and acute myeloid leukemia [J].
Fabre, C. ;
Carvalho, G. ;
Tasdemir, E. ;
Braun, T. ;
Ades, L. ;
Grosjean, J. ;
Boehrer, S. ;
Metivier, D. ;
Souquere, S. ;
Pierron, G. ;
Fenaux, P. ;
Kroemer, G. .
ONCOGENE, 2007, 26 (28) :4071-4083
[8]
Fischer Uwe M, 2006, Interact Cardiovasc Thorac Surg, V5, P531, DOI 10.1510/icvts.2006.130765
[9]
Eat your heart out:: Role of autophagy in myocardial ischemia/reperfusion [J].
Gustafsson, Asa B. ;
Gottlieb, Roberta A. .
AUTOPHAGY, 2008, 4 (04) :416-421
[10]
Autophagy as a protective response to Bnip3-mediated apoptotic signaling in the heart [J].
Hamacher-Brady, Anne ;
Brady, Nathan R. ;
Gottlieb, Roberta A. ;
Gustafsson, Asa B. .
AUTOPHAGY, 2006, 2 (04) :307-309