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SMN1 — TGFB3

Text-mined interactions from Literome

Osaki et al., Int J Exp Pathol 2001 (Pulmonary Fibrosis) : When pulmonary fibroblasts were separated from saline injected rats ( N-Fib ) and cultivated for 7 days in the presence of 5 mg/mL PLM, alpha-SMA protein was weakly expressed, while the majority of pulmonary fibroblasts separated from PLM injected rats ( P-Fib ) became positive for alpha-SMA in 7-day cultivation and the expression of alpha-SMA in P-Fib was strongly increased by cultivation in the presence of PLM and transforming growth factor-beta ( TGF-beta ), but not basic fibroblast growth factor (bFGF) or platelet derived growth factor ( PDGF ), although the cell proliferation was most strongly enhanced by bFGF and only slightly by PLM and TGF-beta
Sandbo et al., Cardiovasc Res 2007 (Shock, Septic) : We show that SMA expression in VSMC, induced by endothelin-1 (ET1) or transforming growth factor-beta ( TGF-beta ), is potently inhibited by a LPS
Nakajima et al., Dev Dyn 1997 : To determine whether TGF beta3 initiates the expression of SMA , the pre-migratory AV endothelial monolayer was cultured with or without chicken recombinant TGF beta3 and the expression of SMA was examined immunochemically ... The induction of the expression of SMA by TGF beta3 is one of the initial events in the cytoskeletal reorganization in endothelial cells which separate from one another during the initial phenotypic change associated with the endothelial-mesenchymal transformation