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SMAD3 — VEGFA

Text-mined interactions from Literome

Nakagawa et al., American journal of physiology. Renal physiology 2004 (Anoxia) : Rat proximal tubular ( NRK52E ) cells treated with TGF-beta under normoxic conditions secreted VEGF at 24 h, and this was significantly reduced by blocking Smad activation by overexpressing the inhibitory Smad7 or by blocking p38 and ERK1/2 MAP kinase activation or protein kinase C activation with specific inhibitors
Sumiyoshi et al., J Invest Dermatol 2004 (Disease Models, Animal...) : Consistent with the in vivo findings, overexpression of Smad3 induced alpha-SMA, VEGF , and TGF-beta1 expression and augmented chemotactic response in cultured dermal fibroblasts
Kobayashi et al., Biochem Biophys Res Commun 2005 : Smad3 mediates TGF-beta1 induction of VEGF production in lung fibroblasts ... These result suggest that TGF-beta1 stimulation of VEGF production by fibroblasts is regulated by Smad3 but not by Smad2 signaling
Yoshida et al., Cell Tissue Res 2007 : In vitro SEC differentiation, as indicated by the appearance of cells co-expressing SE-1 and stabilin-2 and of cells with cytoplasmic fenestrae in endothelial sheets, was induced by the addition of both VEGF and SB-431542, an inhibitor of the phosphorylation of Smad2/3 but not that of Smad1/5/8 in the cultured cells
Chae et al., Oncogene 2011 (Prostatic Neoplasms) : VEGF induction by TGF-ß1 occurred in a Smad3 dependent manner, and the Smad binding element 2 ( SBE2, -992 to -986 ) and hypoxia response element ( -975 to -968 ) in the VEGF promoter were required for the promoter response to TGF-ß1 ... Smad3 cooperated with HIF-2a in TGF-ß1 activation of VEGF transcription and Smad3 binding to the SBE2 site was greatly impaired by knockdown of HIF-2a expression
Lee et al., Cell Tissue Res 2012 (Glomerulonephritis, Membranous...) : Furthermore, activated TGF-ß/Smad signaling by podocytes may induce connective tissue growth factor and vascular endothelial growth factor overexpression, which could act as a paracrine effector mechanism on mesangial cells to stimulate mesangial matrix synthesis
Kajihara et al., Mod Rheumatol 2013 : Furthermore, Smad3 overexpression induced VEGF levels
Farid et al., Toxicol Lett 2013 : Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts ... Silencing of Smad3 by siRNA not only eliminated the stimulatory effect of CSE on VEGF release but also inhibited baseline VEGF production ... Our findings indicate that CSE stimulates Smad3 mediated VEGF release by lung fibroblasts
Bai et al., Development 2013 (Truncus Arteriosus, Persistent...) : Our findings indicate that Smad directly binds to Vegfa chromatin and represses Vegfa transcriptional activity