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Research Article Free access | 10.1172/JCI119457

The cytokine-adhesion molecule cascade in ischemia/reperfusion injury of the rat kidney. Inhibition by a soluble P-selectin ligand.

M Takada, K C Nadeau, G D Shaw, K A Marquette, and N L Tilney

Surgical Research Laboratory, Harvard Medical School and Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Takada, M. in: PubMed | Google Scholar

Surgical Research Laboratory, Harvard Medical School and Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Nadeau, K. in: PubMed | Google Scholar

Surgical Research Laboratory, Harvard Medical School and Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Shaw, G. in: PubMed | Google Scholar

Surgical Research Laboratory, Harvard Medical School and Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Marquette, K. in: PubMed | Google Scholar

Surgical Research Laboratory, Harvard Medical School and Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Tilney, N. in: PubMed | Google Scholar

Published June 1, 1997 - More info

Published in Volume 99, Issue 11 on June 1, 1997
J Clin Invest. 1997;99(11):2682–2690. https://doi.org/10.1172/JCI119457.
© 1997 The American Society for Clinical Investigation
Published June 1, 1997 - Version history
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Abstract

Ischemia/reperfusion (I/R) injury associated with renal transplantation may influence both early graft function and late changes. The initial (</= 7 d) events of warm and in situ perfused cold ischemia of native kidneys in uninephrectomized rats were examined. mRNA expression of the early adhesion molecule, E-selectin, peaked within 6 h; PMNs infiltrated in parallel. T cells and macrophages entered the injured kidney by 2-5 d; the associated upregulation of MHC class II antigen expression suggested increased immunogenicity of the organ. Th1 products (IL-2, TNFalpha, IFNgamma) and macrophage-associated products (IL-1, IL-6, TGFbeta) remained highly expressed after 2 d. To examine directly the effects of selectins in I/R injury, a soluble P-selectin glycoprotein ligand (sPSGL) was used. Ischemic kidneys were perfused in situ with 5 microg of sPSGL in UW solution; 50 microg was administered intravenously 3 h after reperfusion. E-selectin mRNA remained at baseline, leukocytes did not infiltrate the injured organs throughout the 7-d period, and their associated products were markedly inhibited. Class II expression did not increase. No renal dysfunction secondary to I/R occurred. The early changes of I/R injury may be prevented by treatment with soluble P- and E-selectin ligand. This may reduce subsequent host inflammatory responses after transplantation.

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