Activation of HMEC-1 by anti-AT1R and anti-ETAR Ab-positive SSc-IgG on protein and mRNA levels. (A) Dose-dependent IL-8 secretion on different doses of anti-AT1R and anti-ETAR Ab-positive SSc-IgG. Same treatment with NC-IgG failed to demonstrate a dose-dependent IL-8 secretion pattern. (B) Significant increase in IL-8 secretion with SSc-IgG versus NC-IgG and decrease with receptor antagonism (NC-IgG, n = 9, SSc-IgG n = 13, P < 0.05). (C) Increase in IL-8 mRNA levels by SSc-IgG versus NC-IgG (NC-IgG, n = 7, SSc-IgG n = 18, P < 0.05). Receptor antagonism leads to inhibition of IL-8 secretion, as indicated (SSc-IgG, n = 13, P < 0.05, P < 0.01). (D) Increase in VCAM-1 mRNA levels with SSc-IgG compared with NC-IgG (NC-IgG, n = 5, and SSc-IgG, n = 6; P < 0.01) and inhibition by receptor antagonism as indicated (P < 0.05). Mean and SEM, **P < 0.01, and *P < 0.05.
Kill et al. Arthritis Research & Therapy 2014 16:R29 doi:10.1186/ar4457