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Figure 3

From: Complement anaphylatoxins C3a and C5a induce a failing regenerative program in cardiac resident cells. Evidence of a role for cardiac resident stem cells other than cardiomyocyte renewal

Figure 3

CPCs possess functional complement receptors C3aR and C5aR that signal through different pathways. (A) Immunoflourescence de C3aR (FITC) and C5aR(Cy5) on CPCs culture. B) Immunoblot of CPCs to detect C3aR and C5aR receptors. C) Immunoblot of CPCs stimulated with different concentrations of C3a and C5a. C3a C5a stimuli activate PKC, ERK1/2 and NFκB pathways but fail to activate AKT. ERK, AKT and PKC activation are measured as presence phosphorylated forms. NFκB activation is probed as IKK phosphorylation. D) p65 nuclear translocation. Starved CPCs were induced with 100nM C3a or 15 nM C5a, Immunoflorescence of p65 protein reveal nuclear translocation. Serum stimulation is the positive control for activation ERK, AKT and NFkappa Beta. Calcium ionophore is the positive control for PKC activation. MEFS = mouse embryonic fibroblasts, EC = Murine endothelial cell line. IgG Anti C3aR-FITC (green). IgG Anti C5aR-Texas (Red). White bar: 10 μm.

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