Renal ischemic-reperfusion injury in L-selectin-deficient mice

Hamid Rabb, German Ramirez, Sabiha R. Saba, Daniel Reynolds, X. U. Jianchao, Richard Flavell, Scott Antonia

Research output: Contribution to journalArticlepeer-review

Abstract

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-deflcient 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 fields was similar in control and L-selectindeficient 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. Pathophysiological roles of L-selectin in vivo appear to be more complex than in vitro data would suggest. renal ischemia; adhesion; peritonitis.

Original languageEnglish (US)
Pages (from-to)F408-F413
JournalAmerican Journal of Physiology
Volume271
Issue number2 PART 2
DOIs
StatePublished - 1996
Externally publishedYes

ASJC Scopus subject areas

  • Physiology (medical)

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