Expression regulation modulation of intercellular adhension molecular-1 and vascular cell adhension molecule-1 induced by interleukin-1β and tumor necrosis factor-α on fibroblast-like synoviocytes of rheumatoid arthritis

Objective To study the role of protein tyrosine kinase in the expression of intercellular adhension molecule-1 (ICAM-1) and vascular cell adhension molecule-1 (VCAM-1) on fibroblast-like synoviocytes (FLS) of rheumatoid arthritis (RA) stimulated by interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Methods RA FLS were primarily cultured. Western blots were applied to examine transient change of protein tyrosine phosphorylation status in RA FLS stimulated by various dosage of IL-1β and TNF-α. Genistein, the specific protein tyrosine kinase (PTK) inhibitor was used to evaluate the inhibitory role in expression regulation of ICAM-1 and VCAM-1 by IL-1β and TNF-α. Results IL-1β and TNF-α transiently increased protein tyrosine phosphorylation, and up-regulated ICAM-1 and VCAM-1 expression in a dose-dependent manner; genistein, had an obviously inhibitory effect on the expression of VCAM-1, but depressed ICAM-1 expression in mid-degree. Conclusion During signal transduction of IL-1β and TNF-α in RA FLS, tyrosine phosphorylation is increased transiently, PTK has a different role in the up-regulation of ICAM-1 and VCAM-1 induced by IL-1β and TNF-α in RA FLS.