Cardioprotective effects of a novel proteasome inhibitor following ischemia and reperfusion in the isolated perfused rat heart.

@article{Campbell1999CardioprotectiveEO,
  title={Cardioprotective effects of a novel proteasome inhibitor following ischemia and reperfusion in the isolated perfused rat heart.},
  author={B. Campbell and J. Adams and Y. Shin and A. Lefer},
  journal={Journal of molecular and cellular cardiology},
  year={1999},
  volume={31 2},
  pages={
          467-76
        }
}
Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as myocardial injury. These effects are due in large part to endothelial dysfunction leading to an upregulation of cell adhesion molecules and subsequent neutrophil induced cardiac injury. The proteasome inhibitor, PS-519, has been shown to attenuate leukocyte-endothelial cell interactions. We tested the effects of PS-519 on neutrophil mediated cardiac… Expand
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References

SHOWING 1-2 OF 2 REFERENCES
Involvement of platelet-endothelial cell adhesion molecule-1 in neutrophil recruitment in vivo.
TLDR
It appears that PECAM-1 is required for neutrophil transmigration in vivo and may thus be a potential therapeutic target. Expand
Tissue destruction by neutrophils.
  • S. Weiss
  • Medicine
  • The New England journal of medicine
  • 1989
WITH increasing frequency, the human neutrophil is being implicated as a mediator of tissue-destructive events in inflammatory diseases ranging from rheumatoid arthritis and myocardial reperfusionExpand