PMID- 11171688
OWN - NLM
STAT- MEDLINE
DCOM- 20010322
LR  - 20190503
IS  - 0003-4967 (Print)
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 60
IP  - 3
DP  - 2001 Mar
TI  - Insulin-like growth factor 1 blocks collagen release and down regulates matrix 
      metalloproteinase-1, -3, -8, and -13 mRNA expression in bovine nasal cartilage 
      stimulated with oncostatin M in combination with interleukin 1alpha.
PG  - 254-61
AB  - OBJECTIVE: To investigate the effect of insulin-like growth factor 1 (IGF1) on 
      the release of collagen, and the production and expression of matrix 
      metalloproteinases (MMPs) induced by the proinflammatory cytokine interleukin 
      1alpha (IL1alpha) in combination with oncostatin M (OSM) from bovine nasal 
      cartilage and primary human articular chondrocytes. METHODS: Human articular 
      chondrocytes and bovine nasal cartilage were cultured with and without IGF1 in 
      the presence of IL1alpha or IL1alpha + OSM. The release of collagen was measured 
      by an assay for hydroxyproline. Collagenase activity was determined with the 
      diffuse fibril assay using 3H acetylated collagen. The expression of MMP-1, 
      MMP-3, MMP-8, MMP-13, and tissue inhibitor of metalloproteinase 1 (TIMP-1) mRNA 
      was analysed by northern blot. RESULTS: IGF1 can partially inhibit the release of 
      collagen induced by IL1alpha or IL1alpha + OSM from bovine nasal cartilage. This 
      was accompanied by a reduced secretion and activation of collagenase by bovine 
      nasal cartilage. IGF1 can also down regulate IL1alpha or IL1alpha + OSM induced 
      MMP-1, MMP-3, MMP-8, and MMP-13 mRNA expression in human articular chondrocytes 
      and bovine chondrocytes. It had no significant effect on the production and 
      expression of TIMP-1 mRNA in chondrocytes. CONCLUSION: This study shows for the 
      first time that IGF1 can partially block the release of collagen from cartilage 
      and suggests that down regulation of collagenases by IGF1 may be an important 
      mechanism in preventing cartilage resorption initiated by proinflammatory 
      cytokines.
FAU - Hui, W
AU  - Hui W
AD  - Department of Rheumatology, Medical School, University of Newcastle, Newcastle 
      Upon Tyne, NE2 4HH, UK. Wang.Hui@ncl.ac.uk
FAU - Rowan, A D
AU  - Rowan AD
FAU - Cawston, T
AU  - Cawston T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Interleukin-1)
RN  - 0 (OSM protein, human)
RN  - 0 (Peptides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - 106956-32-5 (Oncostatin M)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9007-34-5 (Collagen)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - EC 3.4.24.34 (Matrix Metalloproteinase 8)
RN  - EC 3.4.24.7 (Matrix Metalloproteinase 1)
RN  - RMB44WO89X (Hydroxyproline)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Cartilage/*drug effects/enzymology
MH  - Cattle
MH  - Cells, Cultured
MH  - Chondrocytes/physiology
MH  - Collagen/*metabolism
MH  - Down-Regulation
MH  - Gene Expression
MH  - Humans
MH  - Hydroxyproline/analysis
MH  - Insulin-Like Growth Factor I/*pharmacology/physiology
MH  - Interleukin-1/physiology
MH  - Matrix Metalloproteinase 1/*physiology
MH  - Matrix Metalloproteinase 3/*physiology
MH  - Matrix Metalloproteinase 8/*physiology
MH  - Oncostatin M
MH  - Peptides/physiology
MH  - RNA, Messenger/metabolism
MH  - Tissue Inhibitor of Metalloproteinase-1/physiology
PMC - PMC1753584
EDAT- 2001/02/15 11:00
MHDA- 2001/03/27 10:01
PMCR- 2004/03/01
CRDT- 2001/02/15 11:00
PHST- 2001/02/15 11:00 [pubmed]
PHST- 2001/03/27 10:01 [medline]
PHST- 2001/02/15 11:00 [entrez]
PHST- 2004/03/01 00:00 [pmc-release]
AID - 10.1136/ard.60.3.254 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2001 Mar;60(3):254-61. doi: 10.1136/ard.60.3.254.