title: Protease-activated receptor 2 deficiency reduces cardiac ischemia/reperfusion injury.
abstract: OBJECTIVE
  To investigate the effect of protease-activated receptor (PAR) 2 deficiency on ischemia/reperfusion (I/R) injury-induced infarct size, inflammation, heart remodeling, and cardiac function.
  
  
  RESULTS
  PAR-2 signaling enhances inflammation in different diseases. The effect of PAR-2 deficiency in cardiac I/R injury is unknown. PAR-2(-/-) mice and wild-type littermates were subjected to 30 minutes of ischemia and up to 4 weeks of reperfusion. Infarct size, oxidative/nitrative stress, phosphorylation of mitogen-activated protein kinases, and inflammatory gene expression were assessed 2 hours after reperfusion. Changes in heart size and function were measured by echocardiography up to 4 weeks after reperfusion. Infarct size was significantly reduced in hearts of PAR-2(-/-) mice compared with wild-type littermates. In addition, oxidative/nitrative stress, phosphorylation of mitogen-activated protein kinase, and expression of proinflammatory genes were significantly attenuated in injured hearts of PAR-2(-/-) mice. Finally, PAR-2(-/-) mice were protected from postinfarction remodeling and showed less impairment in heart function compared with wild-type littermates up to 4 weeks after I/R injury.
  
  
  CONCLUSIONS
  PAR-2 deficiency reduces myocardial infarction and heart remodeling after I/R injury.
authors: Division of Hematology/Oncology, Department of Medicine, UNC McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035, USA.
authors: Silvio
authors: S
authors: Antoniak
authors: Mauricio
authors: M
authors: Rojas
authors: Denise
authors: D
authors: Spring
authors: Tara A
authors: TA
authors: Bullard
authors: Edward D
authors: ED
authors: Verrier
authors: Burns C
authors: BC
authors: Blaxall
authors: Nigel
authors: N
authors: Mackman
authors: Rafal
authors: R
authors: Pawlinski
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D004195:Disease Models, Animal; D006333:Heart Failure; D006801:Humans; D007249:Inflammation; D008297:Male; D051379:Mice; D008875:Middle Aged; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D018384:Oxidative Stress; D044464:Receptor, PAR-2 / Q000172:deficiency*; D020257:Ventricular Remodeling
chemical_list: D044464:Receptor, PAR-2