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This Article Full Text Full Text (PDF) All Versions of this Article: 288/2/L227    most recent 00224.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (26) Citing Articles via Google Scholar Google Scholar Articles by Wang, C.-C. Articles by Yang, C.-M. Search for Related Content PubMed PubMed Citation Articles by Wang, C.-C. Articles by Yang, C.-M.

Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-B in IL-1-induced VCAM-1 expression in human tracheal smooth muscle cells

¹Graduate Institute of Natural Products, Departments of ²Pharmacology, ³Anesthetics, and ⁴Internal Medicine, and ⁵Graduate Institute of Rehabilitation Science, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan

Submitted 11 June 2004 ; accepted in final form 20 September 2004

Interleukin-1 (IL-1) has been shown to induce the expression of adhesion molecules on airway epithelial and smooth cells and contributes to inflammatory responses. Here, the roles of mitogen-activated protein kinases (MAPKs) and nuclear factor-B (NF-B) pathways for IL-1-induced vascular cell adhesion molecule (VCAM)-1 expression were investigated in human tracheal smooth muscle cells (HTSMC). IL-1 induced expression of VCAM-1 protein and mRNA in a time-dependent manner, which was significantly inhibited by inhibitors of MEK1/2 (U0126 and PD-98059), p38 (SB-202190), and c-Jun NH₂-terminal kinase (JNK; SP-600125). Consistently, IL-1-stimulated phosphorylation of p42/p44 MAPK, p38, and JNK was attenuated by pretreatment with U0126, SB-202190, or SP-600125, respectively. IL-1-induced VCAM-1 expression was significantly blocked by the specific NF-B inhibitors helenalin and pyrrolidine dithiocarbamate. As expected, IL-1-stimulated translocation of NF-B into the nucleus and degradation of IB- were blocked by helenalin but not by U0126, SB-202190, or SP-600125. Moreover, the resultant enhancement of VCAM-1 expression increased the adhesion of polymorphonuclear cells to a monolayer of HTSMC, which was blocked by pretreatment with helenalin, U0126, SB-202190, or SP-600125 before IL-1 exposure or by anti-VCAM-1 antibody. Together, these results suggest that in HTSMC, activation of p42/p44 MAPK, p38, JNK, and NF-B pathways is essential for IL-1-induced VCAM-1 gene expression. These results provide new insight into the mechanisms of IL-1 action that cytokines may promote inflammatory responses in airway disease.

interleukin-1; mitogen-activated protein kinase; c-Jun NH₂-terminal kinase; nuclear factor-B; vascular cell adhesion molecule-1

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