Renal ischemic-reperfusion injury in L-selectin-deficient mice.
L-selectin on leukocyte surfaces mediates cell rolling on endothelium. L-selectin blockade with antibodies attenuated ischemic-reperfusion injury (IRI) in heart and skeletal muscle, but its role in renal IRI is unknown. We evaluated the role of L-selectin in renal IRI using L-selectin-deficient mice. Neutrophil migration to chemically inflamed peritoneum was reduced by 47% (P < 0.01) in L-selectin-deficient mice. Ischemia was induced by bilateral renal pedicle clamping for 30 min. Control and L-selectin groups had similar elevations of serum creatinine (1.8 +/- 0.3 vs. 1.7 +/- 0.2 mg/dl) and blood urea nitrogen (111 +/- 17 vs. 128 +/- 12 mg/dl) 24 h postischemia. Pathological assessment showed comparable degrees of tubular necrosis at 24 h. The postischemic increase in peritubular neutrophils per 10 high-power field was similar in control and L-selectin-deficient groups at 4 (28 +/- 10 vs. 22 +/- 5), 12 (245 +/- 80 vs. 236 +/- 78), and 24 h (130 +/- 12 vs. 156 +/- 18). These data argue against a significant role for L-selectin in renal IRI. Patho-physiological roles of L-selectin in vivo appear to be more complex than in vitro data would suggest.
Rabb
H
H
Department of Medicine, University of South Florida, Tampa, USA.
Ramirez
G
G
Saba
S R
SR
Reynolds
D
D
Xu
J
J
Flavell
R
R
Antonia
S
S
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D002465:Cell Movement; D006720:Homozygote; D007668:Kidney / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology; D019041:L-Selectin / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008817:Mice, Mutant Strains; D009154:Mutation; D009504:Neutrophils / Q000502:physiology; D010538:Peritonitis / Q000473:pathology; D015427:Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology
D019041:L-Selectin