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PDGFB — SMC6

Text-mined interactions from Literome

Myllärniemi et al., Cardiovasc Drugs Ther 1999 : Administration of the PDGF-R tyrosine kinase inhibitor in vivo, tested and found to inhibit the proliferation of SMC induced by PDGF-AA and PDGF-BB , but not by IGF-1, EGF, or bFGF, resulted in a 60 % reduction in the absolute number and percentage of BrdU + cells after the second balloon injury to pre existing neointima, but had no significant effect on proliferation after the first injury
Facchiano et al., J Cell Sci 2000 : These in vitro studies show that bFGF significantly inhibits PDGF-BB induced SMC migration and proliferation and that this effect is mediated by both PDGF-Ralpha and bFGF receptor
Lu et al., Dev Biol 2001 : We report here that PDGF-BB stimulates EMT and promotes SRF dependent expression of SMC marker genes calponin, SM22alpha, and SMgamma ( actin ) ( SMgammaA ) in proepicardial cells
Dandré et al., Am J Physiol Heart Circ Physiol 2004 : However, there is conflicting evidence whether PDGF-BB represses SMC marker expression at a transcriptional or posttranscriptional level, and little is known regarding the mechanisms responsible for these effects
Hollenbeck et al., Biochem Biophys Res Commun 2004 : PDGF-BB produced a 5.5-fold increase in SMC DNA synthesis whereas CNI stimulated DNA synthesis to a much lesser extent ( 1.6-fold increase )
Liu et al., J Biol Chem 2005 : KLF4 was rapidly up-regulated in PDGF-BB treated, cultured SMC, and a small interfering RNA to KLF4 partially blocked PDGF-BB induced SMC gene repression
Romano et al., J Cell Physiol 2006 : PI3K, ERK, JNK, and p38 kinases, known to mediate PDGF-BB signaling in the canonic dedifferentiative and proliferative response of smooth muscle cells ( SMC ) were rapidly activated by PDGF-BB but only p38 remained activated after 2-day stimulation
Liu et al., J Mol Cell Cardiol 2006 : We have previously reported that PDGF-BB induces the accumulation of monocyte chemoattractant protein (MCP)-1 mRNA in smooth muscle cells ( SMC ) , in large part due to an increase in mRNA stability
Lo et al., Biochem Pharmacol 2007 : Surprisingly, further analysis indicates that lycopene could directly bind PDGF-BB and inhibit PDGF-BB-SMC interaction, as determined by dot binding assay and Western blotting ... One of the action mechanisms is that lycopene is capable of binding PDGF-BB and inhibiting its interaction with SMC , which is quite different from those previously developed PDGFR-beta antagonists
Lamy et al., Carcinogenesis 2008 (Neovascularization, Pathologic) : The inhibitory effect of delphinidin on PDGFR-beta was very rapid and led to the inhibition of PDGF-BB induced activation of extracellular signal regulated kinase ( ERK)-1/2 signaling and of the chemotactic motility of SMC, as well as the differentiation and stabilization of EC and SMC into capillary-like tubular structures in a three-dimensional coculture system
de Mooij et al., Prenat Diagn 2009 (Down Syndrome) : The SMCs surrounding the JLS can possibly be explained by an increase of PDGF-B induced SMC recruitment and/or differentiation
Fukai et al., Arterioscler Thromb Vasc Biol 2009 (Carotid Artery Injuries...) : These results suggest the possibility that syndecan-1 may limit intimal thickening in injured arteries by suppressing SMC activation through inhibition of SMC PDGF-B chain expression and PDGFRbeta activation
Zhang et al., J Biol Chem 2010 : Moreover, we also demonstrated that knockdown of Sp1 abrogated PDGF-BB induced HDAC7 up-regulation and SMC differentiation gene expression in differentiating ES cells, although enforced expression of Sp1 alone was sufficient to increase the activity of the Hdac7 promoter and expression levels of SMC differentiation genes
Dai-Do et al., Cardiovasc Res 1996 : PDGF-BB increased the number of SMC ( P < 0.0001 at 10 days ) obtained from females ( 153 +/- 3 % ; n = 5 ) and males ( 150 +/- 4 % ; n = 5 ), which was inhibited by 17 beta-estradiol ( 10 ( -6 ) M ; female 134 +/- 7 % ; male 128 +/- 5 % ; P < 0.05 )
Mureebe et al., Surgery 1997 : Stimulation of SMC with platelet derived growth factor (PDGF)-BB and AB resulted in an increase in src activation, whereas PDGF-AA did not consistently enhance src activity