Monoclonal antibody to ICAM-1 preserves postischemic blood flow and reduces infarct size after ischemia-reperfusion in rabbit

Zhi, Zhao; Lefer, David J.; Sato, Hiroki; Hart, Kevin K.; Jefforda, P R; Vinten-Johansen, J.

doi:10.1002/jlb.62.3.292

Cited by 74 publications

(39 citation statements)

References 36 publications

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“…PMN inhibition was achieved by leukodepletion using neutrophil antiserum (Kin et al, 2006), or by antibodies targeting adhesion molecules such as P-and E-selectins (Lefer et al, 1994), CD11/CD18 (Ma et al, 1991), intercellular adhesion molecule-1 (Ma et al, 1992;Ioculano et al, 1994;Zhao et al, 1997Zhao et al, , 2003, or platelet/endothelial cell adhesion molecule-1 (Gumina et al, 1996). These strategies provided up to ϳ50% reduction in infarct size.…”

Section: Discussionmentioning

confidence: 99%

A Novel Peptide Agonist of Formyl-Peptide Receptor-Like 1 (ALX) Displays Anti-Inflammatory and Cardioprotective Effects

Hecht¹,

Jiang²,

Sampaio³

et al. 2008

J Pharmacol Exp Ther

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Activation of the formyl-peptide receptor-like (FPRL) 1 pathway has recently gained high recognition for its significance in therapy of inflammatory diseases. Agonism at FPRL1 affords a beneficial effect in animal models of acute inflammatory conditions, as well as in chronic inflammatory diseases. TIPMFVPESTSKLQKFTSWFM-amide (CGEN-855A) is a novel 21-amino acid peptide agonist for FPRL1 and also activates FPRL2. CGEN-855A was discovered using a computational platform designed to predict novel G protein-coupled receptor peptide agonists cleaved from secreted proteins by convertase proteolysis. In vivo, CGEN-855A displays anti-inflammatory activity manifested as 50% inhibition of polymorphonuclear neutrophil (PMN) recruitment to inflamed air pouch and provides protection against ischemia-reperfusion-mediated injury to the myocardium in both murine and rat models (36 and 25% reduction in infarct size, respectively). Both these activities are accompanied by inhibition of PMN recruitment to the injured organ. The secretion of inflammatory cytokines, including interleukin (IL)-6, IL-1␤, and tumor necrosis factor-␣, was not affected upon incubation of human peripheral blood mononuclear cells with CGEN-855A, whereas IL-8 secretion was elevated up to 2-fold upon treatment with the highest CGEN-855A dose only. Collectively, these new data support a potential role for CGEN-855A in the treatment of reperfusionmediated injury and in other acute and chronic inflammatory conditions.

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Section: Discussionmentioning

confidence: 99%

A Novel Peptide Agonist of Formyl-Peptide Receptor-Like 1 (ALX) Displays Anti-Inflammatory and Cardioprotective Effects

Hecht¹,

Jiang²,

Sampaio³

et al. 2008

J Pharmacol Exp Ther

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“…This, in turn, is associated with increased expression of adhesion molecules including ICAM and VCAM (46,47), which can be blocked by proteasome inhibitors (47) or other compounds capable of inhibiting NF-κB activity (40). Furthermore, inhibition of proteasome-mediated IκBα degradation (48) or adhesion molecule expression has been shown to reduce significantly ischemia-reperfusion injury (49)(50)(51).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide

Gao¹,

Lecker²,

Post³

et al. 2000

J. Clin. Invest.

154

124

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“…It is unclear whether the inflammatory response that accompanies an acute MI contributes to the pathogenesis of lethal myocardial reperfusion injury or whether it is a reaction to the acute myocardial injury (42). Although experimental studies have reported significant reduction of MI with therapeutic strategies designed to inhibit the inflammatory process at the time of myocardial reperfusion using antibodies against cell-adhesion molecules (43)(44)(45) and the inhibition of complement activation (46), corresponding clinical studies using this therapeutic approach have been largely negative (47)(48)(49).…”

Section: Figurementioning

confidence: 99%

Myocardial ischemia-reperfusion injury: a neglected therapeutic target

Hausenloy¹,

Yellon²

2013

J. Clin. Invest.

1,821

1,473

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Acute myocardial infarction (MI) is a major cause of death and disability worldwide. In patients with MI, the treatment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy or primary percutaneous coronary intervention (PPCI). However, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. A number of new therapeutic strategies currently under investigation for preventing myocardial reperfusion injury have the potential to improve clinical outcomes in patients with acute MI treated with PPCI.

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Monoclonal antibody to ICAM-1 preserves postischemic blood flow and reduces infarct size after ischemia-reperfusion in rabbit

Abstract: Abstract:Neutrophils are pivotal in the pathogenesis of reperfusion injury leading to myocardial infarction.

Cited by 74 publications

References 36 publications

A Novel Peptide Agonist of Formyl-Peptide Receptor-Like 1 (ALX) Displays Anti-Inflammatory and Cardioprotective Effects

A Novel Peptide Agonist of Formyl-Peptide Receptor-Like 1 (ALX) Displays Anti-Inflammatory and Cardioprotective Effects

Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide

Myocardial ischemia-reperfusion injury: a neglected therapeutic target

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