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Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 expression in human tracheal smooth muscle cells.
Am J Physiol Lung Cell Mol Physiol. 2005 Feb; 288(2):L227-37.AJ

Abstract

Interleukin-1beta (IL-1beta) 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-kappaB (NF-kappaB) pathways for IL-1beta-induced vascular cell adhesion molecule (VCAM)-1 expression were investigated in human tracheal smooth muscle cells (HTSMC). IL-1beta 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 NH(2)-terminal kinase (JNK; SP-600125). Consistently, IL-1beta-stimulated phosphorylation of p42/p44 MAPK, p38, and JNK was attenuated by pretreatment with U0126, SB-202190, or SP-600125, respectively. IL-1beta-induced VCAM-1 expression was significantly blocked by the specific NF-kappaB inhibitors helenalin and pyrrolidine dithiocarbamate. As expected, IL-1beta-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha 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-1beta exposure or by anti-VCAM-1 antibody. Together, these results suggest that in HTSMC, activation of p42/p44 MAPK, p38, JNK, and NF-kappaB pathways is essential for IL-1beta-induced VCAM-1 gene expression. These results provide new insight into the mechanisms of IL-1beta action that cytokines may promote inflammatory responses in airway disease.

Authors+Show Affiliations

Graduate Institute of Natural Products, Department of Pharmacology, 259 Wen-Hwa 1st Road, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15489374

Citation

Wang, Chien-Chun, et al. "Involvement of P42/p44 MAPK, P38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 Expression in Human Tracheal Smooth Muscle Cells." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 288, no. 2, 2005, pp. L227-37.
Wang CC, Lin WN, Lee CW, et al. Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 expression in human tracheal smooth muscle cells. Am J Physiol Lung Cell Mol Physiol. 2005;288(2):L227-37.
Wang, C. C., Lin, W. N., Lee, C. W., Lin, C. C., Luo, S. F., Wang, J. S., & Yang, C. M. (2005). Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 expression in human tracheal smooth muscle cells. American Journal of Physiology. Lung Cellular and Molecular Physiology, 288(2), L227-37.
Wang CC, et al. Involvement of P42/p44 MAPK, P38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 Expression in Human Tracheal Smooth Muscle Cells. Am J Physiol Lung Cell Mol Physiol. 2005;288(2):L227-37. PubMed PMID: 15489374.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB in IL-1beta-induced VCAM-1 expression in human tracheal smooth muscle cells. AU - Wang,Chien-Chun, AU - Lin,Wei-Ning, AU - Lee,Chiang-Wen, AU - Lin,Chih-Chung, AU - Luo,Shue-Fen, AU - Wang,Jong-Shyan, AU - Yang,Chuen-Mao, Y1 - 2004/10/15/ PY - 2004/10/19/pubmed PY - 2005/2/12/medline PY - 2004/10/19/entrez SP - L227 EP - 37 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am. J. Physiol. Lung Cell Mol. Physiol. VL - 288 IS - 2 N2 - Interleukin-1beta (IL-1beta) 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-kappaB (NF-kappaB) pathways for IL-1beta-induced vascular cell adhesion molecule (VCAM)-1 expression were investigated in human tracheal smooth muscle cells (HTSMC). IL-1beta 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 NH(2)-terminal kinase (JNK; SP-600125). Consistently, IL-1beta-stimulated phosphorylation of p42/p44 MAPK, p38, and JNK was attenuated by pretreatment with U0126, SB-202190, or SP-600125, respectively. IL-1beta-induced VCAM-1 expression was significantly blocked by the specific NF-kappaB inhibitors helenalin and pyrrolidine dithiocarbamate. As expected, IL-1beta-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha 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-1beta exposure or by anti-VCAM-1 antibody. Together, these results suggest that in HTSMC, activation of p42/p44 MAPK, p38, JNK, and NF-kappaB pathways is essential for IL-1beta-induced VCAM-1 gene expression. These results provide new insight into the mechanisms of IL-1beta action that cytokines may promote inflammatory responses in airway disease. SN - 1040-0605 UR - https://www.unboundmedicine.com/medline/citation/15489374/Involvement_of_p42/p44_MAPK_p38_MAPK_JNK_and_NF_kappaB_in_IL_1beta_induced_VCAM_1_expression_in_human_tracheal_smooth_muscle_cells_ L2 - http://www.physiology.org/doi/full/10.1152/ajplung.00224.2004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -