Skip to main content
. Author manuscript; available in PMC: 2016 May 18.
Published in final edited form as: J Invest Dermatol. 2015 Aug 19;135(12):3153–3162. doi: 10.1038/jid.2015.323

Figure 4. Defective phosphorylation of FAK in SSc ECs.

Figure 4

a. Phosphorylation of FAK was examined by Western blotting. In normal ECs, VEGF induced significant FAK phosphorylation while in the presence of 8-isoprostane the phosphorylation was inhibited. When the TXAR was knocked down, the inhibitory effect of 8-isoprostane disappeared. In SSc ECs, VEGF failed to induce FAK phosphorylation in the absence or presence of 8-isoprostane. When the TXAR was knocked down, the basal levels of FAK phosphorylation decreased while VEGF and VEGF plus 8-isoprostane groups significantly increased FAK phosphorylation. The extent was still significantly lower compared to the normal ECs. #p<0.05 vs. normal EC control siRNA VEGF group; @p<0.05 vs. normal EC TXAR siRNA NS group; $p<0.05 vs. normal EC TXAR siRNA VEGF group; &p<0.05 vs. normal EC TXAR siRNA VEGF+8-iso group. b-e. The expression of the TXAR, ROCK1/2, and RhoA was examined by qPCR and Western blotting. b. Differences in the TXAR expression did not reach statistical significance at either mRNA or protein levels. c. The expression of ROCK1 was discordant between mRNA and protein levels. ROCK1 protein was significantly higher in SSc ECs. d. Similar to ROCK1, ROCK2 protein expression was significantly higher in SSc ECs. e. Both protein and mRNA levels of RhoA were elevated in SSc ECs compared to normal. Results are expressed as mean ± S.D. and p<0.05 is considered significant. n=number of subjects. 8-iso: 8-isoprostane.