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Interleukin-1beta induces MMP-9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor-kappaB signaling pathways in human tracheal smooth muscle cells.
J Cell Physiol. 2007 Jun; 211(3):759-70.JC

Abstract

Matrix metalloproteinases (MMPs) are responsible for degradation of extracellular matrix and play important roles in cell migration, proliferation, and tissue remodeling related to airway inflammation. Interleukin-1beta (IL-1beta) has been shown to induce MMP-9 production in many cell types and contribute to airway inflammatory responses. However, the mechanisms underlying MMP-9 expression induced by IL-1beta in human tracheal smooth muscle cells (HTSMCs) remain unclear. Here, we investigated the roles of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB pathways for IL-1beta-induced MMP-9 production in HTSMCs. IL-1beta induced production of MMP-9 protein and mRNA in a time- and concentration-dependent manner determined by zymographic, Western blotting, and RT-PCR analyses, which was attenuated by inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), JNK (SP600125), and NF-kappaB (helenalin), and transfection with dominant negative mutants of MEK1/2, p38 and JNK, respectively. IL-1beta-stimulated phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK was attenuated by pretreatment with U0126, SB202190, SP600125, or transfection with these dominant negative mutants of MEK, ERK, p38 and JNK, respectively. Furthermore, IL-1beta-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha was blocked by helenalin. Finally, the reporter gene assay revealed that MAPKs and NF-kappaB are required for IL-1beta-induced MMP-9 luciferase activity in HTSMCs. MMP-9 promoter activity was enhanced by IL-1beta in HTSMCs transfected with MMP-9-Luc, which was inhibited by helenalin, U0126, SB202190, and SP600125. Taken together, the transcription factor NF-kappaB, p42/p44 MAPK, p38 MAPK, and JNK that are involved in MMP-9 expression in HTSMCs exposed to IL-1beta have now been identified.

Authors+Show Affiliations

Liang KC
Department of Physiology and Pharmacology, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan.
Lee CW
No affiliation info available
Lin WN
No affiliation info available
Lin CC
No affiliation info available
Wu CB
No affiliation info available
Luo SF
No affiliation info available
Yang CM
No affiliation info available

MeSH

Cells, CulturedGene Expression Regulation, EnzymologicHumansInterleukin-1betaJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMatrix Metalloproteinase 9Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocytes, Smooth MuscleNF-kappa BPhosphorylationPromoter Regions, GeneticRNA, MessengerTracheap38 Mitogen-Activated Protein Kinases

Pub Type(s)

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

Language

eng

PubMed ID

17311279

Citation

Liang, Kao-Chih, et al. "Interleukin-1beta Induces MMP-9 Expression Via P42/p44 MAPK, P38 MAPK, JNK, and Nuclear factor-kappaB Signaling Pathways in Human Tracheal Smooth Muscle Cells." Journal of Cellular Physiology, vol. 211, no. 3, 2007, pp. 759-70.
Liang KC, Lee CW, Lin WN, et al. Interleukin-1beta induces MMP-9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor-kappaB signaling pathways in human tracheal smooth muscle cells. J Cell Physiol. 2007;211(3):759-70.
Liang, K. C., Lee, C. W., Lin, W. N., Lin, C. C., Wu, C. B., Luo, S. F., & Yang, C. M. (2007). Interleukin-1beta induces MMP-9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor-kappaB signaling pathways in human tracheal smooth muscle cells. Journal of Cellular Physiology, 211(3), 759-70.
Liang KC, et al. Interleukin-1beta Induces MMP-9 Expression Via P42/p44 MAPK, P38 MAPK, JNK, and Nuclear factor-kappaB Signaling Pathways in Human Tracheal Smooth Muscle Cells. J Cell Physiol. 2007;211(3):759-70. PubMed PMID: 17311279.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-1beta induces MMP-9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor-kappaB signaling pathways in human tracheal smooth muscle cells. AU - Liang,Kao-Chih, AU - Lee,Chiang-Wen, AU - Lin,Wei-Ning, AU - Lin,Chih-Chung, AU - Wu,Chou-Bin, AU - Luo,Shue-Fen, AU - Yang,Chuen-Mao, PY - 2007/2/22/pubmed PY - 2007/6/15/medline PY - 2007/2/22/entrez SP - 759 EP - 70 JF - Journal of cellular physiology JO - J Cell Physiol VL - 211 IS - 3 N2 - Matrix metalloproteinases (MMPs) are responsible for degradation of extracellular matrix and play important roles in cell migration, proliferation, and tissue remodeling related to airway inflammation. Interleukin-1beta (IL-1beta) has been shown to induce MMP-9 production in many cell types and contribute to airway inflammatory responses. However, the mechanisms underlying MMP-9 expression induced by IL-1beta in human tracheal smooth muscle cells (HTSMCs) remain unclear. Here, we investigated the roles of p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB pathways for IL-1beta-induced MMP-9 production in HTSMCs. IL-1beta induced production of MMP-9 protein and mRNA in a time- and concentration-dependent manner determined by zymographic, Western blotting, and RT-PCR analyses, which was attenuated by inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), JNK (SP600125), and NF-kappaB (helenalin), and transfection with dominant negative mutants of MEK1/2, p38 and JNK, respectively. IL-1beta-stimulated phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK was attenuated by pretreatment with U0126, SB202190, SP600125, or transfection with these dominant negative mutants of MEK, ERK, p38 and JNK, respectively. Furthermore, IL-1beta-stimulated translocation of NF-kappaB into the nucleus and degradation of IkappaB-alpha was blocked by helenalin. Finally, the reporter gene assay revealed that MAPKs and NF-kappaB are required for IL-1beta-induced MMP-9 luciferase activity in HTSMCs. MMP-9 promoter activity was enhanced by IL-1beta in HTSMCs transfected with MMP-9-Luc, which was inhibited by helenalin, U0126, SB202190, and SP600125. Taken together, the transcription factor NF-kappaB, p42/p44 MAPK, p38 MAPK, and JNK that are involved in MMP-9 expression in HTSMCs exposed to IL-1beta have now been identified. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/17311279/Interleukin_1beta_induces_MMP_9_expression_via_p42/p44_MAPK_p38_MAPK_JNK_and_nuclear_factor_kappaB_signaling_pathways_in_human_tracheal_smooth_muscle_cells_ L2 - https://doi.org/10.1002/jcp.20992 DB - PRIME DP - Unbound Medicine ER -