A Role for galectin-3 in renal tissue damage triggered by ischemia and reperfusion injury

被引:75
作者
Fernandes Bertocchi, Ana Paula [2 ]
Campanhole, Gabriela [2 ]
Mei Wang, Pamella Huey [2 ]
Goncalves, Giselle Martins [2 ]
Damiao, Marcio Jose [2 ]
Cenedeze, Marcos Antonio [2 ]
Beraldo, Felipe Caetano [3 ]
Antunes Teixeira, Vicente de Paula
dos Reis, Marlene Antonia
Mazzali, Marilda [3 ]
Pacheco-Silva, Alvaro [2 ]
Saraiva Camara, Niels Olsen [1 ,2 ]
机构
[1] Univ Sao Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Transplantat Immunol, BR-05508900 Sao Paulo, Brazil
[2] Univ Fed Sao Paulo, Escola Paulista Med, Div Nephrol, Clin & Expt Immunol Lab, Sao Paulo, Brazil
[3] Univ Estadual Campinas, Div Nephrol, Campinas, Brazil
基金
巴西圣保罗研究基金会;
关键词
galectin-3; IL-1; beta; IL-6; ischemia and reperfusion injury; MCP-1;
D O I
10.1111/j.1432-2277.2008.00705.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
Ischemic-reperfusion injury (IRI) triggers an inflammatory response involving neutrophils/macrophages, lymphocytes and endothelial cells. Galectin-3 is a multi-functional lectin with a broad range of action such as promotion of neutrophil adhesion, induction of oxidative stress, mastocyte migration and degranulation, and production of pro-inflammatory cytokines. The aim of this study was evaluate the role of galectin-3 in the inflammation triggered by IRI. Galectin-3 knockout (KO) and wild type (wt) mice were subjected to 45 min of renal pedicle occlusion. Blood and kidney samples were collected at 6, 24, 48 and 120 h. Blood urea was analyzed enzymatically, while MCP-1, IL-6 and IL-1 beta were studied by real-time PCR. Reactive oxygen species (ROS) was investigated by flow cytometry. Morphometric analyses were performed at 6, 24, 48 and 120 h after reperfusion. Urea peaked at 24 h, being significantly lower in knockout animals (wt = 264.4 +/- 85.21 mg/dl vs. gal-3 KO = 123.74 +/- 29.64 mg/dl, P = 0.001). Galectin-3 knockout animals presented less acute tubular necrosis and a more prominent tubular regeneration when compared with controls concurrently with lower expression of MCP-1, IL-6, IL-1 beta, less macrophage infiltration and lower ROS production at early time points. Galectin-3 seems to play a role in renal IRI involving the secretion of macrophage-related chemokine, pro-inflammatory cytokines and ROS production.
引用
收藏
页码:999 / 1007
页数:9
相关论文
共 47 条
[11]   Endoglin regulates renal ischaemia-reperfusion injury [J].
Docherty, Neil G. ;
Lopez-Novoa, Jose M. ;
Arevalo, Miguel ;
Duwel, Annette ;
Rodriguez-Pena, Ana ;
Perez-Barriocanal, Fernando ;
Bernabeu, Carmelo ;
Eleno, Nelida .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2006, 21 (08) :2106-2119
[12]   Purine and cytokine concentrations in the renal vein of the allograft during reperfusion [J].
Domanski, L. ;
Pawlik, A. ;
Safranow, K. ;
Jakubowska, K. ;
Dziedziejko, V. ;
Chlubek, D. ;
Rozanski, J. ;
Myslak, M. ;
Romanowski, M. ;
Sulikowski, T. ;
Sienko, J. ;
Ostrowski, M. ;
Ciechanowski, K. .
TRANSPLANTATION PROCEEDINGS, 2007, 39 (05) :1319-1322
[13]   Inflammatory cells in ischemic acute renal failure [J].
Friedewald, JJ ;
Rabb, H .
KIDNEY INTERNATIONAL, 2004, 66 (02) :486-491
[14]   CCR2 signaling contributes to ischemia-reperfusion injury in kidney [J].
Furuichi, K ;
Wada, T ;
Iwata, Y ;
Kitagawa, K ;
Kobayashi, KI ;
Hashimoto, H ;
Ishiwata, Y ;
Asano, M ;
Wang, H ;
Matsushima, K ;
Takeya, M ;
Kuziel, WA ;
Mukaida, N ;
Yokoyama, H .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2003, 14 (10) :2503-2515
[15]   Interleukin-1-dependent sequential chemokine expression and inflammatory cell infiltration in ischemia-reperfusion injury [J].
Furuichi, Kengo ;
Wada, Takashi ;
Iwata, Yasunori ;
Kokubo, Satoshi ;
Hara, Akinori ;
Yamahana, Junya ;
Sugaya, Takeshi ;
Iwakura, Yoichiro ;
Matsushima, Kouji ;
Asano, Masahide ;
Yokoyama, Hitoshi ;
Kaneko, Shuichi .
CRITICAL CARE MEDICINE, 2006, 34 (09) :2447-2455
[16]   Inflammation-induced modulation of cellular galectin-1 and-3 expression in a model of rat peritonitis [J].
Gil, CD ;
Cooper, D ;
Rosignoli, G ;
Perretti, M ;
Oliani, SM .
INFLAMMATION RESEARCH, 2006, 55 (03) :99-107
[17]   SIMULTANEOUS MEASUREMENT BY FLOW-CYTOMETRY OF PHAGOCYTOSIS AND HYDROGEN-PEROXIDE PRODUCTION OF NEUTROPHILS IN WHOLE-BLOOD [J].
HASUI, M ;
HIRABAYASHI, Y ;
KOBAYASHI, Y .
JOURNAL OF IMMUNOLOGICAL METHODS, 1989, 117 (01) :53-58
[18]   Targeted disruption of the galectin-3 gene results in attenuated peritoneal inflammatory responses [J].
Hsu, DK ;
Yang, RY ;
Pan, ZX ;
Lu, L ;
Salomon, DR ;
Fung-Leung, WP ;
Liu, FT .
AMERICAN JOURNAL OF PATHOLOGY, 2000, 156 (03) :1073-1083
[19]   AN ENDOGENOUS LECTIN, GALECTIN-3 (EPSILON-BP/MAC-2), POTENTIATES IL-1 PRODUCTION BY HUMAN MONOCYTES [J].
JENG, KCG ;
FRIGERI, LG ;
LIU, FT .
IMMUNOLOGY LETTERS, 1994, 42 (03) :113-116
[20]   Macrophages contribute to the initiation of ischaemic acute renal failure in rats [J].
Jo, SK ;
Sung, SA ;
Cho, WY ;
Go, KJ ;
Kim, HK .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2006, 21 (05) :1231-1239