PMID- 19656083
OWN - NLM
STAT- MEDLINE
DCOM- 20100909
LR  - 20211020
IS  - 1768-322X (Electronic)
IS  - 0248-4900 (Print)
IS  - 0248-4900 (Linking)
VI  - 102
IP  - 1
DP  - 2009 Oct 12
TI  - Interleukin-1beta increases gap junctional communication among synovial 
      fibroblasts via the extracellular-signal-regulated kinase pathway.
PG  - 37-49
LID - 10.1042/BC20090056 [doi]
AB  - BACKGROUND INFORMATION: The gap junction protein, Cx43 (connexin 43), has been 
      implicated in the aetiology of osteoarthritis. Studies have revealed that the 
      size and number of gap junctions increase in synovial biopsies from patients with 
      osteoarthritis. Furthermore, pharmacological inhibition of Cx43 function has been 
      shown to reduce IL-1beta (interleukin-1beta)-induced metalloproteinase production 
      by synovial fibroblasts in vitro. RESULTS: In the present study, we examined the 
      link between IL-1beta and Cx43 function. We demonstrated that treatment of a 
      rabbit synovial fibroblast cell line with IL-1beta markedly increased the level 
      of the Cx43 protein in a concentration- and time-dependent manner. The impact on 
      Cx43 protein levels appeared to occur post-transcriptionally, as mRNA levels are 
      unaffected by IL-1beta administration. Additionally, we showed by fluorescence 
      microscopy that IL-1beta alters the cellular distribution of Cx43 to cell-cell 
      junctions and is concomitant with a striking increase in gap junction 
      communication. Furthermore, we demonstrated that the increase in Cx43 protein, 
      and the associated change in protein localization and gap junction communication 
      following IL-1beta treatment, are dependent upon activation of the ERK 
      (extracellular-signal-regulated kinase) signalling cascade. CONCLUSION: These 
      data show that IL-1beta acts through the ERK signalling cascade to alter the 
      expression and function of Cx43 in synovial fibroblasts.
FAU - Niger, Corinne
AU  - Niger C
AD  - Department of Orthopaedics, University of Maryland, School of Medicine, 
      Baltimore, MD 21201, USA.
FAU - Howell, Floyd D
AU  - Howell FD
FAU - Stains, Joseph P
AU  - Stains JP
LA  - eng
GR  - R01 AR052719/AR/NIAMS NIH HHS/United States
GR  - R01 AR052719-04/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20091012
PL  - England
TA  - Biol Cell
JT  - Biology of the cell
JID - 8108529
RN  - 0 (Connexin 43)
RN  - 0 (Interleukin-1beta)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cell Communication/*drug effects
MH  - Cell Line
MH  - Connexin 43/genetics/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Extracellular Signal-Regulated MAP Kinases/*metabolism
MH  - Fibroblasts/*drug effects
MH  - Fluorescent Antibody Technique
MH  - Gap Junctions/*drug effects
MH  - Gene Expression Regulation/drug effects
MH  - Interleukin-1beta/*pharmacology
MH  - Rabbits
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/drug effects
PMC - PMC2874634
MID - NIHMS161448
EDAT- 2009/08/07 09:00
MHDA- 2010/09/10 06:00
PMCR- 2010/10/12
CRDT- 2009/08/07 09:00
PHST- 2009/08/07 09:00 [entrez]
PHST- 2009/08/07 09:00 [pubmed]
PHST- 2010/09/10 06:00 [medline]
PHST- 2010/10/12 00:00 [pmc-release]
AID - BC20090056 [pii]
AID - 10.1042/BC20090056 [doi]
PST - epublish
SO  - Biol Cell. 2009 Oct 12;102(1):37-49. doi: 10.1042/BC20090056.