PMID- 12814617
OWN - NLM
STAT- MEDLINE
DCOM- 20030819
LR  - 20191107
IS  - 1063-4584 (Print)
IS  - 1063-4584 (Linking)
VI  - 11
IP  - 7
DP  - 2003 Jul
TI  - Comparison of the catabolic effects of fibronectin fragments in human knee and 
      ankle cartilages.
PG  - 538-47
AB  - OBJECTIVE: To compare the response of knee and ankle cartilages to fibronectin 
      fragments (Fn-f) in terms of kinetics of matrix proteoglycan (PG) degradation and 
      synthesis, since previous data had shown that knee was more sensitive to Fn-f in 
      terms of steady-state PG content. DESIGN: Human knee and ankle cartilage explants 
      were treated with the 29kDa Fn-f, and its effects on PG-degradation kinetics, on 
      the half-lives of 35S-sulfate-labeled PG, on PG synthesis suppression and on 
      matrix metalloproteinase -3 (MMP-3) were compared. Cultures were also treated 
      with the interleukin (IL) receptor antagonist protein (IRAP) in order to 
      determine whether IL-1 is involved in the Fn-f effect. RESULTS: The Fn-f enhanced 
      PG-degradation rates in both human knee and ankle cartilages. Knee cartilage 
      showed a greater effect of Fn-f on half-lives of newly synthesized 35S-labeled PG 
      than ankle. The extent of release of MMP-3 was similar for human ankle and knee 
      cartilages. However, PG synthesis in knee cartilage was sensitive to 10- to 
      100-fold lower concentrations of Fn-f than was ankle cartilage. IRAP partially 
      reversed Fn-f activity in ankle cartilages. CONCLUSIONS: The role of Fn-f in 
      proteolysis leading to cartilage damage appears to be minor in human cartilages 
      than had previously been shown for bovine. This decreased proteolysis is true for 
      both knee and ankle. The major difference between human ankle and knee cartilage 
      appears to be greater sensitivity to PG synthesis suppression in knee cartilage. 
      A further indication that IL-1 is involved in the pathway was provided by the 
      partial reversal with IRAP.
FAU - Dang, Y
AU  - Dang Y
AD  - Department of Biochemistry, Rush Medical College at Rush-Presbyterian-St. Luke's 
      Medical Center, 1653 West Congress Parkway, Chicago, IL 60612-3864, USA.
FAU - Cole, A A
AU  - Cole AA
FAU - Homandberg, G A
AU  - Homandberg GA
LA  - eng
GR  - 2-P50-AR39239/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Osteoarthritis Cartilage
JT  - Osteoarthritis and cartilage
JID - 9305697
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Fibronectins)
RN  - 0 (IL1RN protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Interleukin-1)
RN  - 0 (Proteoglycans)
RN  - 0 (Sialoglycoproteins)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Ankle Joint/*metabolism
MH  - Antirheumatic Agents/pharmacology
MH  - Cartilage, Articular/*metabolism
MH  - Cells, Cultured
MH  - Female
MH  - Fibronectins/*pharmacology
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Interleukin-1/*physiology
MH  - Knee Joint/*metabolism
MH  - Male
MH  - Matrix Metalloproteinase 3/metabolism
MH  - Middle Aged
MH  - Proteoglycans/*metabolism
MH  - Sialoglycoproteins/pharmacology
EDAT- 2003/06/20 05:00
MHDA- 2003/08/20 05:00
CRDT- 2003/06/20 05:00
PHST- 2003/06/20 05:00 [pubmed]
PHST- 2003/08/20 05:00 [medline]
PHST- 2003/06/20 05:00 [entrez]
AID - S1063458403000852 [pii]
AID - 10.1016/s1063-4584(03)00085-2 [doi]
PST - ppublish
SO  - Osteoarthritis Cartilage. 2003 Jul;11(7):538-47. doi: 
      10.1016/s1063-4584(03)00085-2.