"Additionally, this study provided the first evidence that the NO donor, DEA/NO, could also induce anti-fibrotic actions via a sGC-cGMP-dependent pathway, leading to inhibition of TGF-beta1 signal transduction (at the level of pSmad2) and subsequently, the pro fibrotic influence of TGF-beta1 on renal myofibroblast differentiation, while being able to promote collagen degrading gelatinases (MMP-2 and MMP-9)."
"TGF-beta1 increased the expression of NFYA, TGFbetaR1, TGFbetaR2, p-Smad2, p-Smad3, p-Smad3L, and p-Akt (Ser473), and knocking down NFYA decreased the expression of these genes, except for TGFbetaR2."
"TGFbeta1 increased the mRNA level and protein expression of Smad2, 3, 7 in HSC; it also increased protein expression of collagen I and III."
"As expected, the addition of exogenous TGF-beta1 increased the amount of pSMAD2 produced by BDC2.5 splenocytes, reaching its maximum level at 30-60 minutes after stimulation (data not shown)."
"Our findings suggested that the expression of SOX9, COL10A1 and p-Smad2 was enhanced by TGF-beta1 stimulation in GC cells, further indicating that COL10A1 might play an important role in the TGF-beta1 and Smad2 downstream signaling pathway."
"Previous in vitro studies have identified that TGF-beta1 increased expression of p-Smad2 and collagen content, and converted rat atrial fibroblasts into myofibroblasts, which induced the atrial fibrosis phenotype."
"Exogenous TGF-beta1 induced temporally dependent alterations in Smad2 and Smad3 gene expression."
"Our findings are partly in agreement with a report that TGF-beta1 increased Smad2 mRNA levels without affecting Smad3 mRNA expression [XREF_BIBR]."