Abstract
Protease-activated receptor-2 (PAR-2) is a member of seven transmembrane domain G protein-coupled receptors activated by proteolytic cleavage. PAR-2 is involved in inflammatory events and cardiac ischemic reperfusion injury. The objective of this study was to investigate the effects of PAR-2 in experimental myocardial ischemic preconditioning. To monitor the effects of PAR-2, Langendorff-perfused rat hearts were used. These hearts were treated with PAR-2-activating peptide (PAR-2AP) in various protocols. Hemodynamic parameters (left ventricular developed pressure, left ventricular diastolic pressure, coronary flow rate, and heart rate), several indexes of oxidative injury, and neutrophil accumulation were evaluated. We show for the first time that enhanced PAR-2 activation improves efficiency of ischemic preconditioning and reduces cardiac inflammation in the rat heart. Indeed, after PAR-2AP infusion we found that hemodynamic parameters, oxidative injury, infarct size, and neutrophil accumulation were involved. These data support the concept that PAR-2-dependent cell trafficking may regulate signaling responses to cardiac ischemia and inflammation.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 282 |
| Issue number | 6 51-6 |
| Publication status | Published - 2002 |
Fingerprint
Keywords
- Heart
- Inflammation
ASJC Scopus subject areas
- Physiology
Cite this
Protease-activated receptor-2 activation improves efficiency of experimental ischemic preconditioning. / Napoli, Claudio; De Nigris, Filomena; Cicala, Carla; Wallace, John L.; Caliendo, Giuseppe; Condorelli, Mario; Santagada, Vincenzo; Cirino, Giuseppe.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 282, No. 6 51-6, 2002.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Protease-activated receptor-2 activation improves efficiency of experimental ischemic preconditioning
AU - Napoli, Claudio
AU - De Nigris, Filomena
AU - Cicala, Carla
AU - Wallace, John L.
AU - Caliendo, Giuseppe
AU - Condorelli, Mario
AU - Santagada, Vincenzo
AU - Cirino, Giuseppe
PY - 2002
Y1 - 2002
N2 - Protease-activated receptor-2 (PAR-2) is a member of seven transmembrane domain G protein-coupled receptors activated by proteolytic cleavage. PAR-2 is involved in inflammatory events and cardiac ischemic reperfusion injury. The objective of this study was to investigate the effects of PAR-2 in experimental myocardial ischemic preconditioning. To monitor the effects of PAR-2, Langendorff-perfused rat hearts were used. These hearts were treated with PAR-2-activating peptide (PAR-2AP) in various protocols. Hemodynamic parameters (left ventricular developed pressure, left ventricular diastolic pressure, coronary flow rate, and heart rate), several indexes of oxidative injury, and neutrophil accumulation were evaluated. We show for the first time that enhanced PAR-2 activation improves efficiency of ischemic preconditioning and reduces cardiac inflammation in the rat heart. Indeed, after PAR-2AP infusion we found that hemodynamic parameters, oxidative injury, infarct size, and neutrophil accumulation were involved. These data support the concept that PAR-2-dependent cell trafficking may regulate signaling responses to cardiac ischemia and inflammation.
AB - Protease-activated receptor-2 (PAR-2) is a member of seven transmembrane domain G protein-coupled receptors activated by proteolytic cleavage. PAR-2 is involved in inflammatory events and cardiac ischemic reperfusion injury. The objective of this study was to investigate the effects of PAR-2 in experimental myocardial ischemic preconditioning. To monitor the effects of PAR-2, Langendorff-perfused rat hearts were used. These hearts were treated with PAR-2-activating peptide (PAR-2AP) in various protocols. Hemodynamic parameters (left ventricular developed pressure, left ventricular diastolic pressure, coronary flow rate, and heart rate), several indexes of oxidative injury, and neutrophil accumulation were evaluated. We show for the first time that enhanced PAR-2 activation improves efficiency of ischemic preconditioning and reduces cardiac inflammation in the rat heart. Indeed, after PAR-2AP infusion we found that hemodynamic parameters, oxidative injury, infarct size, and neutrophil accumulation were involved. These data support the concept that PAR-2-dependent cell trafficking may regulate signaling responses to cardiac ischemia and inflammation.
KW - Heart
KW - Inflammation
UR - http://www.scopus.com/inward/record.url?scp=0036087115&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036087115&partnerID=8YFLogxK
M3 - Article
C2 - 12003804
AN - SCOPUS:0036087115
VL - 282
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 6 51-6
ER -