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To determine if other mesodermal lineages emerge using activin A/BMP4 directed differentiation, we performed quantitative RT-PCR for SM22α and VE-cadherin, markers of smooth muscle and endothelium, respectively (Figure S1).
In vessels previously subjected to OPT scanning, (immuno)staining for markers of smooth muscle (α-smooth muscle actin), macrophages (Mac2) and collagen (picro-sirius red) all occurred with the expected intensity and distribution (Figures 2c).
SM22α, also known as transgelin, is a 22-kDa actin-binding protein of the calponin family, a cytoskeleton associated protein and one of the earliest markers of smooth muscle differentiation [ 28, 29].
Although esmolol produces changes in coronary artery structure and function, we cannot conclude that regression of vascular remodeling occurred, because we did not study aspects such as markers of smooth muscle proliferation, activity of matrix metalloproteinases, and staining of perivascular fibrosis.
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Indeed, mRNA encoding Caldesmon (CALD1), a marker of smooth muscle and myofibroblast differentiation, was induced at 24 hours after Wnt3a treatment.
Since enhanced myofibroblast differentiation may explain the acceleration of wound closure in UA2-treated mice, we stained wound tissues at post injury days 5, 8 and 13 with an antibody against alpha smooth muscle actin, a differentiation marker of smooth muscle cells (Fig. 4B, C).
The intracellular marker of smooth muscle cells; αSMA was expressed and had its highest positivity in the PA surrounding vessels.
We have shown that SM22α, an actin-binding protein considered a marker of smooth muscle differentiation, is upregulated in podocytes and PECs in several models of podocyte disease.
The analysis of α-smooth muscle actin (SMA), a marker of smooth muscle cells and pericytes, showed a discontinuous expression in the A-CYLDC/S tumors indicating the immature and leaky nature of the blood vessels.
As an example, smooth muscle actin is frequently adopted as a marker of smooth muscle but can be expressed also by activated myofibroblasts: thus, alone, it is not indicative of bona fide cell differentiation and maturation.
To determine whether the cardiovascular defects observed in the Wnt1cre; Ilk flox/flox mutants were caused by defective differentiation of NCCs into smooth muscle cells, we analyzed the expression of smooth muscle actin (αSMA), a broadly used marker of smooth muscle differentiation.
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