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Interleukin-1beta induces ICAM-1 expression enhancing leukocyte adhesion in human rheumatoid arthritis synovial fibroblasts: involvement of ERK, JNK, AP-1, and NF-kappaB.
J Cell Physiol. 2010 Aug; 224(2):516-26.JC

Abstract

Interleukin-1beta (IL-1beta) has been shown to induce the expression of adhesion molecules on various cell types and contributes to inflammatory responses. However, the molecular mechanisms by which IL-1beta induced intercellular adhesion molecule (ICAM)-1 expression remain unclear in human rheumatoid arthritis synovial fibroblasts (RASFs). Here, we demonstrated that IL-1beta induces ICAM-1 gene expression via the de novo protein synthesis through transcription and translation, which is attenuated by pretreatment with actinomycin D and cycloheximide, respectively. IL-1beta-induced ICAM-1 expression, extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) phosphorylation, AP-1 activation, and nuclear factor-kappaB (NF-kappaB) p65 translocation were attenuated by the inhibitors of MEK1/2 (U0126), JNK (SP600125), AP-1 (tanshinone IIA), and NF-kappaB (helenalin) or transfection with respective short hairpin RNA plasmids. Moreover, IL-1beta-stimulated NF-kappaB p65 translocation was blocked by helenalin, but not by U0126 or SP600125, revealing that MAPKs and NF-kappaB pathways were independent on these responses. IL-1beta-stimulated AP-1 activation was blocked by U0126 or SP600125, revealing that ERK and JNK linked to AP-1 on these responses. IL-1beta-stimulated ICAM-1 gene expression was attenuated by pretreatment with U0126, SP600125, tanshinone IIA, or helenalin, revealed by ICAM-1 promoter assay and real-time RT-PCR analysis. Finally, up-regulation of ICAM-1 enhanced the adhesion of leukocytes to RASFs exposed to IL-1beta. These results suggest that in human RASFs, activation of ERK, JNK, AP-1, and NF-kappaB are essential for IL-1beta-induced ICAM-1 expression and leukocyte adhesion.

Authors+Show Affiliations

Department of Pharmacology, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan. chuenmao@mail.cgu.edu.twNo 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

20432452

Citation

Yang, Chuen-Mao, et al. "Interleukin-1beta Induces ICAM-1 Expression Enhancing Leukocyte Adhesion in Human Rheumatoid Arthritis Synovial Fibroblasts: Involvement of ERK, JNK, AP-1, and NF-kappaB." Journal of Cellular Physiology, vol. 224, no. 2, 2010, pp. 516-26.
Yang CM, Luo SF, Hsieh HL, et al. Interleukin-1beta induces ICAM-1 expression enhancing leukocyte adhesion in human rheumatoid arthritis synovial fibroblasts: involvement of ERK, JNK, AP-1, and NF-kappaB. J Cell Physiol. 2010;224(2):516-26.
Yang, C. M., Luo, S. F., Hsieh, H. L., Chi, P. L., Lin, C. C., Wu, C. C., & Hsiao, L. D. (2010). Interleukin-1beta induces ICAM-1 expression enhancing leukocyte adhesion in human rheumatoid arthritis synovial fibroblasts: involvement of ERK, JNK, AP-1, and NF-kappaB. Journal of Cellular Physiology, 224(2), 516-26. https://doi.org/10.1002/jcp.22153
Yang CM, et al. Interleukin-1beta Induces ICAM-1 Expression Enhancing Leukocyte Adhesion in Human Rheumatoid Arthritis Synovial Fibroblasts: Involvement of ERK, JNK, AP-1, and NF-kappaB. J Cell Physiol. 2010;224(2):516-26. PubMed PMID: 20432452.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-1beta induces ICAM-1 expression enhancing leukocyte adhesion in human rheumatoid arthritis synovial fibroblasts: involvement of ERK, JNK, AP-1, and NF-kappaB. AU - Yang,Chuen-Mao, AU - Luo,Shue-Fen, AU - Hsieh,Hsi-Lung, AU - Chi,Pei-Ling, AU - Lin,Chih-Chung, AU - Wu,Chi-Chuan, AU - Hsiao,Li-Der, PY - 2010/5/1/entrez PY - 2010/5/1/pubmed PY - 2010/6/17/medline SP - 516 EP - 26 JF - Journal of cellular physiology JO - J. Cell. Physiol. VL - 224 IS - 2 N2 - Interleukin-1beta (IL-1beta) has been shown to induce the expression of adhesion molecules on various cell types and contributes to inflammatory responses. However, the molecular mechanisms by which IL-1beta induced intercellular adhesion molecule (ICAM)-1 expression remain unclear in human rheumatoid arthritis synovial fibroblasts (RASFs). Here, we demonstrated that IL-1beta induces ICAM-1 gene expression via the de novo protein synthesis through transcription and translation, which is attenuated by pretreatment with actinomycin D and cycloheximide, respectively. IL-1beta-induced ICAM-1 expression, extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) phosphorylation, AP-1 activation, and nuclear factor-kappaB (NF-kappaB) p65 translocation were attenuated by the inhibitors of MEK1/2 (U0126), JNK (SP600125), AP-1 (tanshinone IIA), and NF-kappaB (helenalin) or transfection with respective short hairpin RNA plasmids. Moreover, IL-1beta-stimulated NF-kappaB p65 translocation was blocked by helenalin, but not by U0126 or SP600125, revealing that MAPKs and NF-kappaB pathways were independent on these responses. IL-1beta-stimulated AP-1 activation was blocked by U0126 or SP600125, revealing that ERK and JNK linked to AP-1 on these responses. IL-1beta-stimulated ICAM-1 gene expression was attenuated by pretreatment with U0126, SP600125, tanshinone IIA, or helenalin, revealed by ICAM-1 promoter assay and real-time RT-PCR analysis. Finally, up-regulation of ICAM-1 enhanced the adhesion of leukocytes to RASFs exposed to IL-1beta. These results suggest that in human RASFs, activation of ERK, JNK, AP-1, and NF-kappaB are essential for IL-1beta-induced ICAM-1 expression and leukocyte adhesion. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/20432452/Interleukin_1beta_induces_ICAM_1_expression_enhancing_leukocyte_adhesion_in_human_rheumatoid_arthritis_synovial_fibroblasts:_involvement_of_ERK_JNK_AP_1_and_NF_kappaB_ L2 - https://doi.org/10.1002/jcp.22153 DB - PRIME DP - Unbound Medicine ER -