Annexin 1 peptides protect against experimental myocardial ischemia‐reperfusion: analysis of their mechanism of action

@article{La2001Annexin1P,
  title={Annexin 1 peptides protect against experimental myocardial ischemia‐reperfusion: analysis of their mechanism of action},
  author={Mylinh La and Michele D'Amico and Silvio Bandiera and Clara Di Filippo and Sonia Maria Oliani and Felicity N. E. Gavins and Roderick John Flower and Mauro Perretti},
  journal={The FASEB Journal},
  year={2001},
  volume={15},
  pages={2247 - 2256}
}
Myocardial reperfusion injury is associated with the infiltration of blood‐borne polymorphonuclear leukocytes. We have previous described the protection afforded by annexin 1 (ANXA1) in an experimental model of rat myocardial ischemia‐reperfu‐sion (IR) injury. We examined the 1) amino acid region of ANXA1 that retained the protective effect in a model of rat heart IR;2) changes in endogenous ANXA1 in relation to the IR induced damage and after pharmacological modulation;and 3) potential… 
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Annexin 1 mimetic peptide protects against renal ischemia/reperfusion injury in rats
TLDR
Results indicate that neutrophils are key mediators for the development of tissue injury after renal ischemia–reperfusion injury and point to an important role of annexin A1 in the epithelial cells defense against I/R injury.
Formyl‐peptide receptor is not involved in the protection afforded by annexin 1 in murine acute myocardial infarct
TLDR
Light is shed on the receptor mechanism(s) mediating annexin 1‐induced cardioprotection and shows a pivotal role for ALX and circulating neutrophil, whereas it excludes any functional involvement of mouse FPR.
Therapeutic Potential of Annexin A1 in Ischemia Reperfusion Injury
TLDR
Mounting evidence suggests that AnxA1, which interacts with the formyl peptide receptor (FPR) family, may have a significant role in mitigating I/RI associated complications.
MC‐3 receptor and the inflammatory mechanisms activated in acute myocardial infarct
TLDR
A previously unrecognized protective role for melanocortin receptor type 3 (MC3‐R) activation on acute and delayed heart reperfusion injury is highlighted, which may open new avenues for therapeutic intervention against heart and possibly other organ ischemia‐reperfusion Injury.
Cardioprotective Actions of the Annexin-A1 N-Terminal Peptide, Ac2-26, Against Myocardial Infarction
TLDR
The data demonstrate the first evidence that Ac2-26 not only preserves cardiomyocyte survival in vitro, but also offers cardioprotection beyond the first few hours after an ischemic insult in vivo.
Annexin A1 Reduces Inflammatory Reaction and Tissue Damage Through Inhibition of Phospholipase A2 Activation in Adult Rats Following Spinal Cord Injury
TLDR
The results, particularly the improvements obtained in tissue sparing and electrophysiologic measures, suggest a neuroprotective effect of ANXA1.
Ac2-26, an Annexin A1 Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury
TLDR
Results indicated that Ac2-26 had a protective effect against acute lung injury induced by IR, which may be via the activation of the FPR.
Annexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice
TLDR
The data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma.
Annexin‐1 peptide Anx‐12–26 protects adult rat cardiac myocytes from cellular injury induced by simulated ischaemia
TLDR
The annexin‐1 peptide Anx‐12–26 potently prevents cardiac myocyte injury induced by metabolic inhibition, an action that was dependent at least in part on the activation of the formyl peptide receptor family of G‐protein‐coupled receptors, protein kinase C, p38 mitogen‐activated protein Kinase and ATP‐sensitive potassium channels.
Cardioprotective potential of annexin-A1 mimetics in myocardial infarction.
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