ANTIBODIES TO ICAM-1 PROTECT KIDNEYS IN SEVERE ISCHEMIC REPERFUSION INJURY

被引:127
作者
RABB, H
MENDIOLA, CC
SABA, SR
DIETZ, JR
SMITH, CW
BONVENTRE, JV
RAMIREZ, G
机构
[1] UNIV S FLORIDA,DEPT INTERNAL MED,TAMPA,FL 33612
[2] UNIV S FLORIDA,DEPT PATHOL,TAMPA,FL 33612
[3] UNIV S FLORIDA,DEPT PHYSIOL,TAMPA,FL 33612
[4] JAMES A HALEY VET HOSP,TAMPA,FL 33612
[5] BAYLOR COLL MED,HOUSTON,TX 77030
[6] MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02129
关键词
D O I
10.1006/bbrc.1995.1779
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
ICAM-1 has been implicated in the pathophysiology of ischemic-reperfusion injury in a number of organs, but its role in mediating severe ischemic-reperfusion injury in the kidney has not been extensively studied. Uninephrectomized Sprague Dawley rats were pretreated with either control monoclonal antibody (mAb) or mAb to ICAM-1 and subjected to 60 min of renal artery occlusion. The serum creatinine, complete blood count and kidney histo-pathological damage scores (PDS) (Scale:0-4) were assessed prior to and 24 hours after ischemia. Mean serum creatinine (mg/dl) 24 hours after ischemia was significantly decreased in the anti-ICAM-1 group (1.38 +/- 0.23, p<0.001) compared to control (2.87 +/- 0.34). PDS was also reduced in anti-ICAM-1 (2.55 +/- 0.20, p<0.05) group compared to control (3.35 +/- 0.30). These data demonstrate that blocking ICAM-1 significantly mitigates severe ischemic acute renal failure, findings which may lead to improved therapy for this condition. (C) 1995 Academic Press, Inc.
引用
收藏
页码:67 / 73
页数:7
相关论文
共 17 条
[1]   MECHANISMS OF ISCHEMIC ACUTE-RENAL-FAILURE [J].
BONVENTRE, JV .
KIDNEY INTERNATIONAL, 1993, 43 (05) :1160-1178
[2]  
CHASSON A L, 1960, Tech Bull Regist Med Technol, V30, P207
[3]  
COSIMI AB, 1990, J IMMUNOL, V144, P4604
[4]  
HARLAN JM, 1992, ADHESION ITS ROLE IN, P117
[5]  
KAWASAKI K, 1993, J IMMUNOL, V150, P1074
[6]   ANTIBODY TO INTERCELLULAR-ADHESION MOLECULE-1 PROTECTS THE KIDNEY AGAINST ISCHEMIC-INJURY [J].
KELLY, KJ ;
WILLIAMS, WW ;
COLVIN, RB ;
BONVENTRE, JV .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (02) :812-816
[7]   POSTISCHEMIC RENAL INJURY IS MEDIATED BY NEUTROPHILS AND LEUKOTRIENES [J].
KLAUSNER, JM ;
PATERSON, IS ;
GOLDMAN, G ;
KOBZIK, L ;
RODZEN, C ;
LAWRENCE, R ;
VALERI, CR ;
SHEPRO, D ;
HECHTMAN, HB .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 256 (05) :F794-F802
[8]   REQUIREMENTS FOR LEUKOCYTE ADHESION MOLECULES IN NEPHROTOXIC NEPHRITIS [J].
MULLIGAN, MS ;
JOHNSON, KJ ;
TODD, RF ;
ISSEKUTZ, TB ;
MIYASAKA, M ;
TAMATANI, T ;
SMITH, CW ;
ANDERSON, DC ;
WARD, PA .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (02) :577-587
[9]   NEUTROPHIL-DEPENDENT ACUTE LUNG INJURY - REQUIREMENT FOR P-SELECTIN (GMP-140) [J].
MULLIGAN, MS ;
POLLEY, MJ ;
BAYER, RJ ;
NUNN, MF ;
PAULSON, JC ;
WARD, PA .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (04) :1600-1607
[10]   OXYGEN FREE-RADICALS IN ISCHEMIC ACUTE-RENAL-FAILURE IN THE RAT [J].
PALLER, MS ;
HOIDAL, JR ;
FERRIS, TF .
JOURNAL OF CLINICAL INVESTIGATION, 1984, 74 (04) :1156-1164