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Figure 7

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 7

Effects of complement anaphylatoxins upon stemness myofibroblast and cardiogenic potential of CPCs. A) C3a and C5a induces expression of miofibroblast transcription factors (SM22a, myocardin, TCF21, α-SMA) and markers (Vimentin, Collagen and Desmin). In other hand reduces expression of endothelial genes (CD31, vWF and E-Cadherin). Genes involved in endMT (Twist1, Snail and Fsp1) are also induced. There is an increase in cardiogenic genes as NKx2.5, Actc1, Tbx5 and Tbx3. But Gata4 is repressed. B) Complement anaphylatoxins induce myofibroblast differentiation. Treatment with C3a and C5a produces a marked increase in the mRNA levels of core factors involved in myofibroblast differentiation (Myocardin, SM22alpha, TCF21) as well as in the mRNA levels of the mature myofibroblast markers SM-actin, Desmin, Vimentin, and Col1a. B) Immunofluorescence confirms data presented in B; CPCs treated with C3a or C5a present higher number of cells positive for SMA. As a positive control for endothelial differentiation, CPCs were cultured in Endothelial Media (EGM); in A) cells cultured in this condition repress the expression of myofibroblast and endMT associated genes and induce the expression of the endothelial markers. p ≤ 0.05 (*); p ≤ 0.01 (**).

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