Nitric oxide synthase 2 is required for conversion of pro-fibrogenic inflammatory CD133+ progenitors into F4/80+ macrophages in experimental autoimmune myocarditis | Zendy

Przemysław Błyszczuk | Zendy; Corrine Berthonneche | Zendy; Silvia Behnke | Zendy; Marcel Glönkler | Zendy; Holger Moch | Zendy; Thierry Pedrazzini | Zendy; Thomas F. Lüscher | Zendy; Urs Eriksson | Zendy; Gabriela Kania | Zendy

Open Access

Nitric oxide synthase 2 is required for conversion of pro-fibrogenic inflammatory CD133+ progenitors into F4/80+ macrophages in experimental autoimmune myocarditis

Author(s) -

Przemysław Błyszczuk,

Corrine Berthonneche,

Silvia Behnke,

Marcel Glönkler,

Holger Moch,

Thierry Pedrazzini,

Thomas F. Lüscher,

Urs Eriksson,

Gabriela Kania

Publication year - 2012

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvs317

Subject(s) - myocarditis , nitric oxide synthase , nitric oxide , progenitor cell , immunology , chemistry , medicine , inflammation , microbiology and biotechnology , biology , stem cell

Experimental autoimmune myocarditis (EAM) model mirrors important mechanisms of inflammatory dilated cardiomyopathy (iDCM). In EAM, inflammatory CD133(+) progenitors are a major cellular source of cardiac myofibroblasts in the post-inflammatory myocardium. We hypothesized that exogenous delivery of macrophage-colony-stimulating factor (M-CSF) can stimulate macrophage lineage differentiation of inflammatory progenitors and, therefore, prevent their naturally occurring myofibroblast fate in EAM.

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