Disease-modifying effects of glucosamine HCl involving regulation of metalloproteinases and chemokines activated by interleukin-1β in human primary synovial fibroblasts

Hsien-Tsung Lu, Yu Chih Liang, Ming Thau Sheu, Hsiu O. Ho, Ya Ting Lin, Ming-Shium Hsieh, Chien Ho Chen

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13 Citations (Scopus)

Abstract

The purpose of this study was to investigate the possible involvement of synovium in cartilage destruction in osteoarthritis (OA) patients. Using human primary synovial fibroblasts (HPSFs), we examined the effects of glucosamine (GLN) on the regulation of the expression of matrix metalloproteinases (MMP-1, -2, and -13) and chemokines (IL-8, MCP-1, and RANTES) as well as the involvement of MAPK signal pathways (JNK, ERK, and p-38) and the transcription factor of NF-κB on the present or absence of interleukin (IL)-1β. Our experiments showed that protein production and mRNA expressions of MMP-1, MMP-3, MMP-13, IL-8, MCP-1, and RANTES were downregulated by treatment with glucosamine in HPSFs. The results further showed that GLN could inhibit IκBα phosphorylation and IκBα degradation leading to inhibition of the translocation of NF-κB to nuclei. However, GLN upregulated MAPKs pathways in HPSFs cells with or without IL-1β. The results suggest that the inhibition of MMP-1, -3, and -13 expressions as well as IL-8, MCP-1, and RANTES productions by GLN might mediate suppression of NF-κB signal pathways, and HPSFs seem to have a potential functions as an alternative source of MMPs and chemokines for inducing the degradation of cartilage in OA.

Original languageEnglish
Pages (from-to)38-50
Number of pages13
JournalJournal of Cellular Biochemistry
Volume104
Issue number1
DOIs
Publication statusPublished - May 1 2008

Fingerprint

Glucosamine
Metalloproteases
Fibroblasts
Matrix Metalloproteinases
Interleukin-1
Chemokines
Chemokine CCL5
Interleukin-8
Osteoarthritis
Cartilage
Signal Transduction
Matrix Metalloproteinase 1
Synovial Membrane
Degradation
Phosphorylation
Transcription Factors
Down-Regulation
Messenger RNA
Proteins

Keywords

  • Glucosamine
  • Matrix metalloproteinases
  • Osteoarthritis
  • Synovial fibroblasts

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

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title = "Disease-modifying effects of glucosamine HCl involving regulation of metalloproteinases and chemokines activated by interleukin-1β in human primary synovial fibroblasts",
abstract = "The purpose of this study was to investigate the possible involvement of synovium in cartilage destruction in osteoarthritis (OA) patients. Using human primary synovial fibroblasts (HPSFs), we examined the effects of glucosamine (GLN) on the regulation of the expression of matrix metalloproteinases (MMP-1, -2, and -13) and chemokines (IL-8, MCP-1, and RANTES) as well as the involvement of MAPK signal pathways (JNK, ERK, and p-38) and the transcription factor of NF-κB on the present or absence of interleukin (IL)-1β. Our experiments showed that protein production and mRNA expressions of MMP-1, MMP-3, MMP-13, IL-8, MCP-1, and RANTES were downregulated by treatment with glucosamine in HPSFs. The results further showed that GLN could inhibit IκBα phosphorylation and IκBα degradation leading to inhibition of the translocation of NF-κB to nuclei. However, GLN upregulated MAPKs pathways in HPSFs cells with or without IL-1β. The results suggest that the inhibition of MMP-1, -3, and -13 expressions as well as IL-8, MCP-1, and RANTES productions by GLN might mediate suppression of NF-κB signal pathways, and HPSFs seem to have a potential functions as an alternative source of MMPs and chemokines for inducing the degradation of cartilage in OA.",
keywords = "Glucosamine, Matrix metalloproteinases, Osteoarthritis, Synovial fibroblasts, Glucosamine, Matrix metalloproteinases, Osteoarthritis, Synovial fibroblasts",
author = "Hsien-Tsung Lu and Liang, {Yu Chih} and Sheu, {Ming Thau} and Ho, {Hsiu O.} and Lin, {Ya Ting} and Ming-Shium Hsieh and Chen, {Chien Ho}",
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T1 - Disease-modifying effects of glucosamine HCl involving regulation of metalloproteinases and chemokines activated by interleukin-1β in human primary synovial fibroblasts

AU - Lu, Hsien-Tsung

AU - Liang, Yu Chih

AU - Sheu, Ming Thau

AU - Ho, Hsiu O.

AU - Lin, Ya Ting

AU - Hsieh, Ming-Shium

AU - Chen, Chien Ho

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N2 - The purpose of this study was to investigate the possible involvement of synovium in cartilage destruction in osteoarthritis (OA) patients. Using human primary synovial fibroblasts (HPSFs), we examined the effects of glucosamine (GLN) on the regulation of the expression of matrix metalloproteinases (MMP-1, -2, and -13) and chemokines (IL-8, MCP-1, and RANTES) as well as the involvement of MAPK signal pathways (JNK, ERK, and p-38) and the transcription factor of NF-κB on the present or absence of interleukin (IL)-1β. Our experiments showed that protein production and mRNA expressions of MMP-1, MMP-3, MMP-13, IL-8, MCP-1, and RANTES were downregulated by treatment with glucosamine in HPSFs. The results further showed that GLN could inhibit IκBα phosphorylation and IκBα degradation leading to inhibition of the translocation of NF-κB to nuclei. However, GLN upregulated MAPKs pathways in HPSFs cells with or without IL-1β. The results suggest that the inhibition of MMP-1, -3, and -13 expressions as well as IL-8, MCP-1, and RANTES productions by GLN might mediate suppression of NF-κB signal pathways, and HPSFs seem to have a potential functions as an alternative source of MMPs and chemokines for inducing the degradation of cartilage in OA.

AB - The purpose of this study was to investigate the possible involvement of synovium in cartilage destruction in osteoarthritis (OA) patients. Using human primary synovial fibroblasts (HPSFs), we examined the effects of glucosamine (GLN) on the regulation of the expression of matrix metalloproteinases (MMP-1, -2, and -13) and chemokines (IL-8, MCP-1, and RANTES) as well as the involvement of MAPK signal pathways (JNK, ERK, and p-38) and the transcription factor of NF-κB on the present or absence of interleukin (IL)-1β. Our experiments showed that protein production and mRNA expressions of MMP-1, MMP-3, MMP-13, IL-8, MCP-1, and RANTES were downregulated by treatment with glucosamine in HPSFs. The results further showed that GLN could inhibit IκBα phosphorylation and IκBα degradation leading to inhibition of the translocation of NF-κB to nuclei. However, GLN upregulated MAPKs pathways in HPSFs cells with or without IL-1β. The results suggest that the inhibition of MMP-1, -3, and -13 expressions as well as IL-8, MCP-1, and RANTES productions by GLN might mediate suppression of NF-κB signal pathways, and HPSFs seem to have a potential functions as an alternative source of MMPs and chemokines for inducing the degradation of cartilage in OA.

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