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suppression of endothelial cell activity by inhibition of tnfαtnfα抑制内皮细胞活性的抑制
Shu et al. Arthritis Research Therapy 2012, 14:R88
/content/14/2/R88
RESEARCH ARTICLE Open Access
Suppression of endothelial cell activity by
inhibition of TNFa
1,2 2 2 2 2,3*
Qiang Shu , Mohammad A Amin , Jeffrey H Ruth , Phillip L Campbell and Alisa E Koch
Abstract
Introduction: TNFa is a proinflammatory cytokine that plays a central role in the pathogenesis of rheumatoid
arthritis (RA). We investigated the effects of certolizumab pegol, a TNFa blocker, on endothelial cell function and
angiogenesis.
Methods: Human dermal microvascular endothelial cells (HMVECs) were stimulated with TNFa with or without
certolizumab pegol. TNFa-induced adhesion molecule expression and angiogenic chemokine secretion were
measured by cell surface ELISA and angiogenic chemokine ELISA, respectively. We also examined the effect of
certolizumab pegol on TNFa-induced myeloid human promyelocytic leukemia (HL-60) cell adhesion to HMVECs, as
well as blood vessels in RA synovial tissue using the Stamper-Woodruff assay. Lastly, we performed HMVEC
chemotaxis, and tube formation.
Results: Certolizumab pegol significantly blocked TNFa-induced HMVEC cell surface angiogenic E-selectin, vascular
cell adhesion molecule-1 and intercellular adhesion molecule-1 expression and angiogenic chemokine secretion (P
0.05). We found that certolizumab pegol significantly inhibited TNFa-induced HL-60 cell adhesion to HMVECs (P
0.05), and blocked HL-60 cell adhesion to RA synovial tissue vasculature (P 0.05). TNFa also enhanced HMVEC
chemotaxis compared with the negative control group (P 0.05) and this chemotactic response was significantly
reduced by certolizumab pegol (P 0.05). Certolizumab pegol inhibited TNFa-induced HMVEC
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