Skip to main content
. 2021 Sep 29;24(10):103193. doi: 10.1016/j.isci.2021.103193

Figure 6.

Figure 6

SMOC2 induces kidney fibrosis by cross-activating signaling cascades of TGFβ, Integrin, MAPKs, and Akt

(A) Western blots showing collagen 1 production in response to several stimuli at 24 h. Note that SMOC2 stimulation markedly increases collagen 1 expression. ALK5/TGFβR II inhibitor of GW788388 (10 μM), ALK5 inhibitor of SB431542 (10 μM), and TGFβR I/II inhibitor of LY2109761 (10 μM) block the SMOC2 (100 ng/mL, 24 h)-induced collagen 1 expression.

(B) Western blots show that SMOC2 (100 ng/mL, 24 h)-induced collagen 1 responses of the different inhibitors, integrin α5 antagonist of ATN-121 (100 μM) and integrin antagonist of SB273005 (1 μM).

(C) Western blots show the effects of inhibition of different signaling pathways on the SMOC2-induced collagen 1 expression with p42/44-MAPK inhibition (U0126 [10 μM]), p38-MAPK inhibition (SB203580 [10 μM]), JNK/SAPK inhibition (SP600125 [10 μM]), and PI3K/Akt inhibition (LY294002 [20 μM]).

(D and E) Immunostaining for F-Actin shows effects on NIH/3T3 of co-stimulation of SMOC2 (100 ng/mL, 24 h) with inhibitors or antagonists (U0126, SP600125, SB203580, LY294002, LY2109761, GW788388, SB431542, SB273005). Positive controls consisted of predicted modulation of TGFβ1 (10 ng/mL, 24 h) stimulation and cascades inhibitors (SB431542, LY2109761, GW788388). Immunofluorescence staining with 40x magnification and scale bar, 20 μm. Images and blots are representative of three independent experiments.