Tags

Type your tag names separated by a space and hit enter

Induction of dental pulp fibroblast matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression by interleukin-1alpha and tumor necrosis factor-alpha through a prostaglandin-dependent pathway.
J Endod. 2001 Mar; 27(3):185-9.JE

Abstract

Matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) are involved in the degradation of extracellular matrix in many inflammatory diseases. Little is known regarding the expression of these mediators in dental pulp fibroblasts. The effects of proinflammatory cytokines (interleukin (IL)-1alpha and tumor necrosis factor-alpha (TNF-alpha)) and prostaglandin E2 (PGE2) on pulp fibroblast MMP-1 and TIMP-1 gene expression were investigated. Northern hybridization showed that IL-1alpha and TNF-alpha induced significant MMP-1 gene expression, with only little effect on TIMP-1 gene. Exogenous PGE2, however, upregulated TIMP-1 mRNA synthesis but not MMP-1. Concomitant addition of IL-1alpha and PGE2 or TNF-alpha and PGE2 suppressed MMP-1 mRNA production, compared with the groups treated with IL-1alpha or TNF-alpha alone. In contrast, PGE2 enhanced the upregulatory effects of TIMP-1 mRNA by IL-1alpha or TNF-alpha. Furthermore, cytokine stimulation of MMP-1 and TIMP-1 gene expressions can be enhanced or blocked by indomethacin, respectively, and reversed by exogenous PGE2. These results suggested that cytokine-stimulated MMP-1 and TIMP-1 gene expression in dental pulp fibroblasts was mediated, at least in part, by a prostaglandin-dependent pathway. The differential regulation of IL-1alpha or TNF-alpha-induced MMP-1 and TIMP-1 mRNA synthesis, as well as the direct upregulation of TIMP-1 gene expression by PGE2, also implied that prostaglandin may serve as a protective mechanism from excessive tissue breakdown during pulpitis.

Authors+Show Affiliations

School of Dentistry, Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

11487149

Citation

Lin, S K., et al. "Induction of Dental Pulp Fibroblast Matrix Metalloproteinase-1 and Tissue Inhibitor of Metalloproteinase-1 Gene Expression By Interleukin-1alpha and Tumor Necrosis Factor-alpha Through a Prostaglandin-dependent Pathway." Journal of Endodontics, vol. 27, no. 3, 2001, pp. 185-9.
Lin SK, Wang CC, Huang S, et al. Induction of dental pulp fibroblast matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression by interleukin-1alpha and tumor necrosis factor-alpha through a prostaglandin-dependent pathway. J Endod. 2001;27(3):185-9.
Lin, S. K., Wang, C. C., Huang, S., Lee, J. J., Chiang, C. P., Lan, W. H., & Hong, C. Y. (2001). Induction of dental pulp fibroblast matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression by interleukin-1alpha and tumor necrosis factor-alpha through a prostaglandin-dependent pathway. Journal of Endodontics, 27(3), 185-9.
Lin SK, et al. Induction of Dental Pulp Fibroblast Matrix Metalloproteinase-1 and Tissue Inhibitor of Metalloproteinase-1 Gene Expression By Interleukin-1alpha and Tumor Necrosis Factor-alpha Through a Prostaglandin-dependent Pathway. J Endod. 2001;27(3):185-9. PubMed PMID: 11487149.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of dental pulp fibroblast matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression by interleukin-1alpha and tumor necrosis factor-alpha through a prostaglandin-dependent pathway. AU - Lin,S K, AU - Wang,C C, AU - Huang,S, AU - Lee,J J, AU - Chiang,C P, AU - Lan,W H, AU - Hong,C Y, PY - 2001/8/7/pubmed PY - 2001/10/12/medline PY - 2001/8/7/entrez SP - 185 EP - 9 JF - Journal of endodontics JO - J Endod VL - 27 IS - 3 N2 - Matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) are involved in the degradation of extracellular matrix in many inflammatory diseases. Little is known regarding the expression of these mediators in dental pulp fibroblasts. The effects of proinflammatory cytokines (interleukin (IL)-1alpha and tumor necrosis factor-alpha (TNF-alpha)) and prostaglandin E2 (PGE2) on pulp fibroblast MMP-1 and TIMP-1 gene expression were investigated. Northern hybridization showed that IL-1alpha and TNF-alpha induced significant MMP-1 gene expression, with only little effect on TIMP-1 gene. Exogenous PGE2, however, upregulated TIMP-1 mRNA synthesis but not MMP-1. Concomitant addition of IL-1alpha and PGE2 or TNF-alpha and PGE2 suppressed MMP-1 mRNA production, compared with the groups treated with IL-1alpha or TNF-alpha alone. In contrast, PGE2 enhanced the upregulatory effects of TIMP-1 mRNA by IL-1alpha or TNF-alpha. Furthermore, cytokine stimulation of MMP-1 and TIMP-1 gene expressions can be enhanced or blocked by indomethacin, respectively, and reversed by exogenous PGE2. These results suggested that cytokine-stimulated MMP-1 and TIMP-1 gene expression in dental pulp fibroblasts was mediated, at least in part, by a prostaglandin-dependent pathway. The differential regulation of IL-1alpha or TNF-alpha-induced MMP-1 and TIMP-1 mRNA synthesis, as well as the direct upregulation of TIMP-1 gene expression by PGE2, also implied that prostaglandin may serve as a protective mechanism from excessive tissue breakdown during pulpitis. SN - 0099-2399 UR - https://www.unboundmedicine.com/medline/citation/11487149/Induction_of_dental_pulp_fibroblast_matrix_metalloproteinase_1_and_tissue_inhibitor_of_metalloproteinase_1_gene_expression_by_interleukin_1alpha_and_tumor_necrosis_factor_alpha_through_a_prostaglandin_dependent_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0099-2399(05)60731-5 DB - PRIME DP - Unbound Medicine ER -