PMID- 20662071
OWN - NLM
STAT- MEDLINE
DCOM- 20101130
LR  - 20220121
IS  - 1529-0131 (Electronic)
IS  - 0004-3591 (Linking)
VI  - 62
IP  - 11
DP  - 2010 Nov
TI  - Cartilage tissue enhances proteoglycan retention by nucleus pulposus cells in 
      vitro.
PG  - 3395-403
LID - 10.1002/art.27651 [doi]
AB  - OBJECTIVE: To investigate the effect of cartilage on nucleus pulposus (NP) tissue 
      in an in vitro model. METHODS: Cells were isolated from bovine NP or articular 
      cartilage and allowed to form tissue in vitro. The NP tissue was grown either 
      alone or in the presence of cartilage tissue (coculture) for up to 4 weeks and 
      examined for histologic appearance, gene expression, and biochemical composition. 
      For selected experiments, NP tissue was grown in coculture with fragments of 
      cartilage end-plate. RESULTS: Coculture of in vitro-formed NP tissue with 
      cartilage end-plate tissue resulted in a significant increase in proteoglycan 
      content in the NP tissue by 2 weeks, compared with NP tissue grown alone. 
      Substituting in vitro-formed cartilage tissue for cartilage end-plate also had a 
      positive effect on the NP tissue, suggesting that it was an appropriate 
      substitute for cartilage end-plate. Coculture of NP with in vitro-formed 
      cartilage for 2 weeks increased aggrecan and collagen gene expression compared 
      with that in NP tissue grown alone, and also reduced expression of matrix 
      metalloproteinase 3 (MMP-3), MMP-13, and ADAMTS-5. NP cells from older and 
      younger animals responded similarly to in vitro-formed cartilage. Expression of 
      genes for tumor necrosis factor alpha (TNFalpha) and TACE in NP cells was higher when 
      grown in the absence of cartilage. This corresponded with increased TNFalpha protein 
      levels in the absence of cartilage. CONCLUSION: The data suggest that 
      chondrocytes may secrete a factor(s) that positively enhances tissue growth, 
      perhaps by inhibiting TNFalpha production. This could be a potential mechanism 
      explaining how loss of the cartilage end-plate may contribute to the development 
      of NP degenerative changes.
CI  - Copyright (c) 2010 by the American College of Rheumatology.
FAU - Arana, Claudia J
AU  - Arana CJ
AD  - Mount Sinai Hospital and University of Toronto, Toronto, Ontario, Canada.
FAU - Diamandis, Eleftherios P
AU  - Diamandis EP
FAU - Kandel, Rita A
AU  - Kandel RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Aggrecans)
RN  - 0 (Proteoglycans)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - ADAM Proteins/metabolism
MH  - Aggrecans/metabolism
MH  - Analysis of Variance
MH  - Animals
MH  - Blotting, Western
MH  - Cartilage/*metabolism
MH  - Cattle
MH  - Chondrocytes/metabolism
MH  - Coculture Techniques
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Intervertebral Disc/*metabolism
MH  - Matrix Metalloproteinases/metabolism
MH  - Proteoglycans/*metabolism
MH  - Tissue Culture Techniques
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2010/07/28 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/07/28 06:00
PHST- 2010/07/28 06:00 [entrez]
PHST- 2010/07/28 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
AID - 10.1002/art.27651 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2010 Nov;62(11):3395-403. doi: 10.1002/art.27651.