fig2

Figure 2. Regulation of smooth muscle cell phenotypes. Smooth muscle cells usually exist in a contractile differentiated state characterized by expression of contractile proteins, such as α-SMA, SM22-α, calponin and smoothelin. This is regulated by the SRF-myocardin transcription complex in response to extracellular and intracellular cues. Dedifferenitation into a synthetic phenotype is driven by the inhibition of the SRF-myocardin system via KLF4. RhoA and ROCKs play a role in both of these pathways. α-SMA: Alpha smooth muscle actin; ECM: extracellular matrix; GPCR: G protein-coupled receptor; KLF4: Kruppel-like factor 4; LIMK: LIM domain kinase; mDia: mammalian diaphanous-related formin; MLC: myosin light chain; MRTF: myocardin-related transcription factor; NFκB: nuclear factor kappa B; PDGF-BB: platelet-derived growth factor-BB; PDGF-Rβ: platelet-derived growth factor-BB receptor beta; RGS: regulator of G protein signaling; ROCK: Rho kinase; SM22-α: smooth muscle 22 alpha; SRF: serum-response factor; TGFβ: transforming growth factor beta; TGFBRII: transforming growth factor beta receptor two.