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Smooth muscle α-actin, the most commonly used marker of myofibroblast differentiation, was also found to be significantly upregulated by Wnt3a (Figure 4C).
See Figure 3. α-SMA is commonly used as a marker of myofibroblast formation [ 13].
α-SMA expression is considered to be a useful marker of myofibroblast differentiation in several disease settings [ 31]–[ 34].
Immunostaining for u-PA, u-PAR, CD68 (monocyte and macrophage marker), α-SMA (the most widely observed marker of myofibroblast formation) and α2AP were performed as follows.
The organization of αSMA stress fibers can be visualized via immunostaining and is the most well accepted marker of myofibroblast activation.
TGFβ1 markedly increased alpha-smooth muscle actin (α-SMA; a marker of myofibroblast formation) and the ECM proteins fibronectin and collagen I at both mRNA and protein levels.
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Consistently, the expression of α-smooth muscle actin (α-SMA), a marker of myofibroblasts (Lin et al., 2009), decreased remarkably in the fibrotic kidney of RBP-J cKO mice as determined using immunohischemistry staining (Fig. 1A lower panel and 1C).
As α-SMA is a putative cell marker of myofibroblasts [23], this result suggests that P311 may induce the myofibroblast phenotype.
This was confirmed using an antibody against α−smooth muscle actin (α−SMA), a marker of myofibroblasts and FRCs [24] (Figure 2, G I).
16 Desmin has also been used as a negative marker of myofibroblasts.
We next investigated the expression of α-SMA, a marker of myofibroblasts, in UUO kidneys.
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