Importantly, co-staining of p-STAT3 with smooth muscle marker proteins (α-smooth muscle actin) revealed high expression levels of p-STAT3 in neointimal SMCs and also of smooth muscle-like cells in the adventitial layer (Suppl. Fig. 1a).
Compounds 3d and 3f also decreased the levels of signature extracellular matrix marker proteins (fibronectin, collagen, and α-smooth muscle actin) and representative mesenchymal cell markers (N-cadherin and vimentin).
Interestingly, Cav-1 KO VSMC show elevated proliferation, DNA synthesis and cell migration although they clearly express the smooth muscle contractile marker proteins calponin and SM22, suggesting that Cav-1-dependent hyper-proliferation does not involve a transition from a contractile to a synthetic phenotype, as demonstrated in VSMCs stimulated to proliferate with e.g. FBS and PDGF [ 20, 28].
Moreover, overexpression of miR-128 led to decreased expression of SMC cellular marker proteins, such as smooth muscle actin (SMA) and calponin, in TGF-β1-induced SMC differentiation.
Since cell types of two different germ lineages were present within the cultures after the neuronal differentiation, the expression of neuronal and smooth muscle lineage marker proteins and of the progenitor marker nestin were quantified.
Prolonged exposure of rabbit ASMCs to muscarinic agonists decreases the expression of smooth muscle specific marker proteins, down-regulates muscarinic receptors and decreases ASMC contractile responsiveness.
The phenotype of the A7r5 aortic smooth muscle cells grown on the different PEMU surfaces was assessed by determining expression of smooth muscle cell "synthetic" and "contractile" phenotype marker proteins and ability to produce contractile force.
Lane 1 marker proteins; lane 2 NecC.
Triangles in b indicate elution positions of marker proteins.
We immunoprecipitated H2A and probed for H2A125Kme1 and the associated heterochromatin marker protein HP1α in HEK-AT1R and vascular smooth muscle cells.
