Involvement of Oxidative Stress in Protective Cardiac Functions of Calprotectin
Luc Rochette,
Geoffrey Dogon,
Eve Rigal,
Marianne Zeller,
Yves Cottin,
Catherine Vergely
Affiliations
Luc Rochette
Equipe d’Accueil (EA 7460): Physiopathologie et Epidémiologie Cérébro-Cardiovasculaires (PEC2), Faculté des Sciences de Santé, Université de Bourgogne—Franche Comté, 7 Bd Jeanne d’Arc, 21000 Dijon, France
Geoffrey Dogon
Equipe d’Accueil (EA 7460): Physiopathologie et Epidémiologie Cérébro-Cardiovasculaires (PEC2), Faculté des Sciences de Santé, Université de Bourgogne—Franche Comté, 7 Bd Jeanne d’Arc, 21000 Dijon, France
Eve Rigal
Equipe d’Accueil (EA 7460): Physiopathologie et Epidémiologie Cérébro-Cardiovasculaires (PEC2), Faculté des Sciences de Santé, Université de Bourgogne—Franche Comté, 7 Bd Jeanne d’Arc, 21000 Dijon, France
Marianne Zeller
Equipe d’Accueil (EA 7460): Physiopathologie et Epidémiologie Cérébro-Cardiovasculaires (PEC2), Faculté des Sciences de Santé, Université de Bourgogne—Franche Comté, 7 Bd Jeanne d’Arc, 21000 Dijon, France
Yves Cottin
Service de Cardiologie, CHU-Dijon, 21000 Dijon, France
Catherine Vergely
Equipe d’Accueil (EA 7460): Physiopathologie et Epidémiologie Cérébro-Cardiovasculaires (PEC2), Faculté des Sciences de Santé, Université de Bourgogne—Franche Comté, 7 Bd Jeanne d’Arc, 21000 Dijon, France
Calprotectin (CLP) belonging to the S-100 protein family is a heterodimeric complex (S100A8/S100A9) formed by two binding proteins. Upon cell activation, CLP stored in neutrophils is released extracellularly in response to inflammatory stimuli and acts as damage-associated molecular patterns (DAMPs). S100A8 and S100A9 possess both anti-inflammatory and anti-bacterial properties. The complex is a ligand of the toll-like receptor 4 (TLR4) and receptor for advanced glycation end (RAGE). At sites of infection and inflammation, CLP is a target for oxidation due to its co-localization with neutrophil-derived oxidants. In the heart, oxidative stress (OS) responses and S100 proteins are closely related and intimately linked through pathophysiological processes. Our review summarizes the roles of S100A8, S100A9 and CLP in the inflammation in relationship with vascular OS, and we examine the importance of CLP for the mechanisms driving in the protection of myocardium. Recent evidence interpreting CLP as a critical modulator during the inflammatory response has identified this alarmin as an interesting drug target.