Bond, Horace M.

Reperfusion‐induced myocardial dysfunction is prevented by endogenous annexin‐A1 and its N‐terminal‐derived peptide Ac‐ANX‐A12‐26

“…for treating I-R injury. In addition to their established inhibition of the systemic inflammatory response (D'Amico et al, 2000;La et al, 2001;Gavins et al, 2005;Hecht et al, 2009), ANX-A1 analogues address damage by acting directly on the myocardium, limiting its ability to contract and relax, as evidenced by our own observations, as well as preventing cardiomyocyte death, an important determinant of outcome from MI (Murphy and Steenbergen, 2008;Peart and Headrick, 2009). Furthermore, this protection is effective when treatment is initiated subsequent to the injury.…”

“…The myocardium can be further damaged by ischaemic contracture, resulting in incomplete recovery of left ventricular (LV) function as reperfusion ensues (Moens et al, 2005;Goh et al, 2007;Li et al, 2009;Venardos et al, 2009;Tawa et al, 2010). Although the previous studies of Perretti, Gavins and colleagues have shown that ANX-A1 peptides powerfully limit neutrophil-dependent myocardial necrosis (D'Amico et al, 2000;La et al, 2001;Gavins et al, 2005;, their effect specifically on post-ischaemic recovery of LV contractile function is unknown. Interventions that preserve LV contractile function following an ischaemic insult may be particularly relevant clinically, and affect prognosis.…”

Annexin‐A1: a pivotal regulator of the innate and adaptive immune systems

“…injections, into rats, rabbits or mice, of amounts (mg) of (usually) the hu-r-Anx-A1 itself or peptides containing the active N terminus suppress inflammatory hyperalgesia (Ferreira et al, 1997), fever (Carey et al, 1990;Davidson et al, 1991;Strijbos et al, 1992), carrageenin paw oedema (Miele et al, 1988;Cirino et al, 1989;Browning et al, 1990;Arcone et al, 1993), zymosan peritonitis (Getting et al, 1997) and cell migration (Perretti and Flower, 1993b;Perretti et al, 1993aPerretti et al, , 1996Mancuso et al, 1995;Allcock et al, 2001) or attachment to the vessel wall (Lim et al, 1998). Anx-A1 mitigates the outcome of NMDA-induced damage of the brain (Black et al, 1992) as well as ischaemiareperfusion injury in the brain (Relton et al, 1991;Rothwell and Relton, 1993;Gavins et al, 2007), myocardium (D'Amico et al, 2000;La et al, 2001a, b;Gavins et al, 2005) and mesentery (Cuzzocrea et al, 1997). In many of these studies, the acute inhibitory actions of glucocorticoids were blunted or abolished by pretreatment with anti-Anx-A1-neutralizing antisera, providing presumptive evidence for the involvement of Anx-A1 in their action.…”