PMID- 10090156
OWN - NLM
STAT- MEDLINE
DCOM- 19990507
LR  - 20131121
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 26
IP  - 3
DP  - 1999 Mar
TI  - Downregulation of intercellular adhesion molecule-1 expression on human synovial 
      fibroblasts by endothelin-1.
PG  - 522-31
AB  - OBJECTIVE: To study the effect of endothelin-1 (ET-1) on the expression of 
      intercellular adhesion molecule-1 (ICAM-1) by synovial fibroblasts derived from 
      individuals with rheumatoid arthritis (RA) or osteoarthritis (OA). METHODS: The 
      expression of ICAM-1 protein and the abundance of ICAM-1 mRNA in synovial 
      fibroblasts derived from individuals with RA or OA, or healthy controls, was 
      assessed by flow cytometry and Northern blot analysis, respectively. mRNA 
      expression of ET type A (ETA) and ET type B (ETB) receptors was assessed by 
      reverse transcription polymerase chain reaction. RESULTS: Tumor necrosis 
      factor-alpha (TNF-alpha) increased the expression of ICAM-1 by RA and OA 
      fibroblasts. While ET-1 alone had no significant effect on ICAM-1 expression by 
      either cell type, it inhibited the TNF-alpha induced increase in ICAM-1 
      expression, and this effect was more marked in RA fibroblasts. TNF-alpha also 
      increased the amount of ICAM-1 mRNA in both cell types, and ET-1 inhibited this 
      increase to a greater extent in RA fibroblasts than in OA fibroblasts. This 
      inhibitory effect of ET-1 was reversed by addition of specific antagonist of ETA 
      receptor. mRNA expression of ETA and ETB receptors was significantly greater in 
      RA fibroblasts stimulated with TNF-alpha or even medium alone than in OA 
      fibroblasts. CONCLUSION: These results suggest that ICAM-1 expression by 
      fibroblasts is regulated not only by proinflammatory cytokines such as TNF-alpha 
      and interleukin-1beta, but also by the vasoactive peptide ET-1, and that ET-1 may 
      play an important role in inflammatory responses, especially in rheumatoid 
      synovitis.
FAU - Iwabuchi, H
AU  - Iwabuchi H
AD  - First Department of Internal Medicine, Showa University School of Medicine, 
      Tokyo, Japan.
FAU - Kasama, T
AU  - Kasama T
FAU - Hanaoka, R
AU  - Hanaoka R
FAU - Miwa, Y
AU  - Miwa Y
FAU - Hatano, Y
AU  - Hatano Y
FAU - Kobayashi, K
AU  - Kobayashi K
FAU - Mori, Y
AU  - Mori Y
FAU - Negishi, M
AU  - Negishi M
FAU - Ide, H
AU  - Ide H
FAU - Adachi, M
AU  - Adachi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (DNA Primers)
RN  - 0 (Endothelin-1)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Endothelin A)
RN  - 0 (Receptor, Endothelin B)
RN  - 0 (Receptors, Endothelin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 1CC1JFE158 (Dactinomycin)
RN  - 98600C0908 (Cycloheximide)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/metabolism
MH  - Cells, Cultured
MH  - Cycloheximide/pharmacology
MH  - DNA Primers/chemistry
MH  - Dactinomycin/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Down-Regulation
MH  - Endothelin-1/*pharmacology
MH  - Female
MH  - Fibroblasts/*drug effects/metabolism
MH  - Flow Cytometry
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - Intercellular Adhesion Molecule-1/*biosynthesis/genetics
MH  - Interleukin-1/pharmacology
MH  - Male
MH  - Middle Aged
MH  - Osteoarthritis/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Receptor, Endothelin A
MH  - Receptor, Endothelin B
MH  - Receptors, Endothelin/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Synovial Membrane/cytology/*drug effects/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1999/03/25 00:00
MHDA- 1999/03/25 00:01
CRDT- 1999/03/25 00:00
PHST- 1999/03/25 00:00 [pubmed]
PHST- 1999/03/25 00:01 [medline]
PHST- 1999/03/25 00:00 [entrez]
PST - ppublish
SO  - J Rheumatol. 1999 Mar;26(3):522-31.