PMID- 18061975
OWN - NLM
STAT- MEDLINE
DCOM- 20080311
LR  - 20080107
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 35
IP  - 1
DP  - 2008 Jan
TI  - Regulation of tenascin-C expression by tumor necrosis factor-alpha in cultured 
      human osteoarthritis chondrocytes.
PG  - 147-52
AB  - Expression of tenascin-C reappears in articular cartilage of persons with 
      osteoarthritis (OA), while it is almost abolished in normal mature cartilage. 
      Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is 
      upregulated in OA cartilage and is involved in the progression of OA, and 
      stimulates tenascin-C expression in other types of cells. We investigated 
      regulation of tenascin-C expression by TNF-alpha through nuclear factor-alphaB 
      (NF-kappaB) in OA cartilage in vivo and in vitro. METHODS: Human articular 
      cartilages were obtained from patients with OA and immunofluorescence examination 
      of tenascin-C and the activated RelA subunit was performed. Cultured chondrocytes 
      isolated from human OA cartilage were treated with TNF-alpha and with SN50. 
      Activation of RelA subunit of NF-kappaB was examined by immunolabeling. Changes 
      in tenascin-C protein concentrations were determined by immunofluorescence of 
      cells after monensin treatment and Western blot analysis of the cell lysates, and 
      mRNA levels were analyzed by quantitative real-time polymerase chain reaction. 
      RESULTS: Increased intensity of tenascin-C staining was observed in the damaged 
      cartilage compared with normal cartilage. Activated RelA staining in chondrocyte 
      nuclei was prominent in tenascin-C-positive areas of OA cartilage. Treatment of 
      cultured chondrocytes by TNF-alpha induced translocation of activated RelA to the 
      nuclei, followed by upregulation of tenascin-C expression in both mRNA and 
      protein. Treatment with SN50 inhibited increases of RelA and tenascin-C 
      expression in chondrocytes. CONCLUSION: TNF-alpha stimulated tenascin-C 
      expression through NF-kappaB signaling with RelA activation in cultured OA 
      chondrocytes, suggesting involvement of tenascin-C in OA cartilage remodeling.
FAU - Nakoshi, Yutaka
AU  - Nakoshi Y
AD  - Department of Orthopedic Surgery and Department of Pathology and Matrix Biology, 
      Mie University Graduate School of Medicine, Mie, Japan.
FAU - Hasegawa, Masahiro
AU  - Hasegawa M
FAU - Sudo, Akihiro
AU  - Sudo A
FAU - Yoshida, Toshimichi
AU  - Yoshida T
FAU - Uchida, Atsumasa
AU  - Uchida A
LA  - eng
PT  - Journal Article
DEP - 20071201
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Tenascin)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Cartilage/physiopathology
MH  - Case-Control Studies
MH  - Cells, Cultured
MH  - Chondrocytes/*metabolism
MH  - Femur/cytology
MH  - Humans
MH  - Middle Aged
MH  - Osteoarthritis/*metabolism/physiopathology
MH  - Tenascin/*metabolism
MH  - Transcription Factor RelA/*metabolism
MH  - Tumor Necrosis Factor-alpha/*physiology
MH  - Up-Regulation
EDAT- 2007/12/07 09:00
MHDA- 2008/03/12 09:00
CRDT- 2007/12/07 09:00
PHST- 2007/12/07 09:00 [pubmed]
PHST- 2008/03/12 09:00 [medline]
PHST- 2007/12/07 09:00 [entrez]
AID - 07/13/127 [pii]
PST - ppublish
SO  - J Rheumatol. 2008 Jan;35(1):147-52. Epub 2007 Dec 1.