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B in Interleukin-1
-induced VCAM-1 Expression in Human Tracheal Smooth Muscle Cells
1 Graduate Institute of natrual Products, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan
2 Department of Pharmacology, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan
3 Department of Anesthetics, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan
4 Department of Internal Medicine, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan
5 Graduate Institute of rehabilitation Asicence, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan
6 Graduate Institute of natrual Products, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan; Department of Pharmacology, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan
* To whom correspondence should be addressed. E-mail: chuenmao{at}mail.cgu.edu.tw.
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 PD98059), p38 (SB202190), and c-Jun-N-terminal kinase (JNK; SP600125). Consistently, IL-1-stimulated phosphorylation of p42/p44 MAPK, p38,
and JNK was attenuated by pretreatment with U0126, SB202190, or SP600125, respectively. IL-1-induced VCAM-1 expression was significantly blocked by
specific NF-B inhibitors helenalin and PDTC. As expected, IL-1-stimulated translocation of NF-B into the nucleus and degradation of IB-
was blocked by helenalin, but not by U0126, SB202190, or SP600125. Moreover, the resultant enhancement of VCAM-1 expression increased the adhesion of polymorphonuclear cells to monolayer of HTSMC which was blocked by pretreatment with helenalin, U0126, SB202190, or SP600125 prior to IL-1 exposure or by anti-VCAM-1 antibody. Taken 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 the airway disease.
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