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. 2021 Aug 19;17(13):3583–3594. doi: 10.7150/ijbs.61647

Figure 7.

Figure 7

The overexpression of Arkadia induces the loss of Smad7 and promotes the effect of recombinant latent TGF-β1 protein on high glucose-induced fibrosis and inflammation in cells, which inhibits Arkadia-mediated Smad7 degradation. (A) Overexpression of Arkadia in mesangial cells. (B) The level of Smad7 decreased in mouse mesangial cells overexpressing Arkadia. (C) The addition of latent TGF-β1 to cells overexpressing Arkadia increased Smad7, which inhibited the fibrosis marker (fibronectin and Col IV) and inflammation marker (IL-1β) as well as inhibited the phosphorylation of Smad3 and NF-κB p65. LG, low glucose (5.5 mM D-glucose). HG, high glucose (35 mM D-glucose). LT1, recombinant latent TGF-β1 protein (20 ng/ml). EV, Empty vector. OE, Overexpression. Data represent the means ± SEM from 3-4 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 versus EV-LG control; #P < 0.05, ##P < 0.01, ###P < 0.001 versus EV-HG treatment. $P < 0.05, $$P < 0.01, $$$ P < 0.001 versus OE-LG control. ^P < 0.05, ^^P < 0.01, ^^^P < 0.001 versus OE-HG treatment.