PMID- 17226782
OWN - NLM
STAT- MEDLINE
DCOM- 20070613
LR  - 20220321
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 211
IP  - 3
DP  - 2007 Jun
TI  - Injury of skeletal muscle and specific cytokines induce the expression of gap 
      junction channels in mouse dendritic cells.
PG  - 649-60
AB  - Dendritic cells (DCs) in culture express at least connexin43, a protein subunit 
      of gap junctions, and form gap junction channels, which could be important for 
      T-cells activation. Here, we evaluated whether DCs express connexins in vivo and 
      also to identify components of their microenvironment that regulate the 
      functional expression of gap junctions. In vivo studies were performed in lymph 
      nodes of mice under control conditions or after skeletal muscle damage. In double 
      immunolabeling studies, connexin45 was frequently detected in DEC205(+) DCs in 
      lymph nodes of control animals, whereas connexin43 was rarely found in DCs. 
      However, connexin43 was upregulated in DCs after skeletal muscle damage. 
      Upregulation of connexin43 gene expression by tissue damage was also confirmed in 
      mice carrying a beta-galactosidase reporter gene in a connexin43 allele. The 
      effect of several cytokines on the expression of functional gap junctions between 
      cultured DCs was also tested. Under control conditions, cultured DCs did not 
      communicate via gap junctions. However, after treatment with 
      keratinocyte-conditioned medium or cytokine mixtures containing at least 
      TNF-alpha and IL-1beta, they became transiently coupled through a pathway 
      sensitive to octanol, a gap junction blocker. Cellular coupling induced by 
      effective cytokine mixtures was prevented by IL-6. Single cytokines (TNF-alpha, 
      IL-1beta, IFN-gamma, or IL-6) or other mixtures than the described above did not 
      induce coupling via gap junctions. Increased levels of connexin43 and connexin45 
      protein and mRNA accompanied the appearance of cellular coupling. These studies 
      provide demonstration of connexin expression and regulation by specific danger 
      signals in DCs.
FAU - Corvalan, Liliana A
AU  - Corvalan LA
AD  - Departamento de Ciencias Fisiologicas, Pontificia Universidad Catolica de Chile, 
      Santiago, Chile.
FAU - Araya, Roberto
AU  - Araya R
FAU - Branes, Maria C
AU  - Branes MC
FAU - Saez, Pablo J
AU  - Saez PJ
FAU - Kalergis, Alexis M
AU  - Kalergis AM
FAU - Tobar, Jaime A
AU  - Tobar JA
FAU - Theis, Martin
AU  - Theis M
FAU - Willecke, Klaus
AU  - Willecke K
FAU - Saez, Juan C
AU  - Saez JC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Connexin 43)
RN  - 0 (Connexins)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (connexin 45)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Cell Communication/drug effects/immunology
MH  - Cell Line
MH  - Connexin 43/*genetics
MH  - Connexins/*genetics
MH  - Culture Media, Conditioned/pharmacology
MH  - Cytokines/*pharmacology
MH  - Dendritic Cells/cytology/*physiology
MH  - Gap Junctions/physiology
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-1beta/pharmacology
MH  - Interleukin-6/pharmacology
MH  - Keratinocytes/cytology
MH  - Lymph Nodes/cytology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Mutant Strains
MH  - Muscle, Skeletal/*immunology/*injuries
MH  - RNA, Messenger/metabolism
MH  - Signal Transduction/drug effects/immunology
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Up-Regulation/physiology
EDAT- 2007/01/18 09:00
MHDA- 2007/06/15 09:00
CRDT- 2007/01/18 09:00
PHST- 2007/01/18 09:00 [pubmed]
PHST- 2007/06/15 09:00 [medline]
PHST- 2007/01/18 09:00 [entrez]
AID - 10.1002/jcp.20971 [doi]
PST - ppublish
SO  - J Cell Physiol. 2007 Jun;211(3):649-60. doi: 10.1002/jcp.20971.