PMID- 9799450
OWN - NLM
STAT- MEDLINE
DCOM- 19981216
LR  - 20231213
IS  - 0302-766X (Print)
IS  - 0302-766X (Linking)
VI  - 294
IP  - 2
DP  - 1998 Nov
TI  - Downregulation of connexin32 protein and gap-junctional intercellular 
      communication by cytokine-mediated acute-phase response in immortalized mouse 
      hepatocytes.
PG  - 345-50
AB  - In the present study, we have analyzed the direct effects of cytokines, which 
      mediate the acute-phase response in liver, on connexin expression and 
      gap-junctional intercellular communication in immortalized MHSV12 mouse 
      hepatocytes. When these cells were stimulated for 24 h with interleukin 1 and 
      interleukin 6, the amount of connexin26 (Cx26) mRNA increased together with 
      beta-fibrinogen mRNA, as expected for this positive acute-phase gene. In 
      contrast, connexin32 (Cx32) mRNA expression was not affected under these 
      conditions. Indirect immunfluorescence revealed a drastic decrease in Cx32 
      signals, whereas slightly more Cx26 signals were found. Stronger stimulation with 
      interleukin 1 and tumor necrosis factor alpha gave a dose-dependent increase in 
      steady state levels of Cx26 and beta-fibrinogen mRNA, but no further change in 
      Cx32 mRNA level was seen. However, when Cx32 protein was analyzed on immunoblots, 
      we found a 5-fold decrease in expression even at low cytokine doses that did not 
      affect Cx32 mRNA expression. Under these conditions, cell to cell transfer of 
      Lucifer yellow, microinjected into immortalized hepatocytes, was decreased by 
      70%, suggesting that intercellular communication through Cx32 channels was 
      partially inhibited earlier than other genetic alterations characteristic of the 
      acute-phase response. Thus, the major hepatic gap junction protein was largely 
      downregulated at the beginning of the experimental inflammatory reaction, but 
      about 30% of gap-junctional intercellular communication was maintained. This 
      suggests that, during the acute-phase response, the second hepatic Cx26 protein 
      may compensate in part for the downregulation of the Cx32 protein.
FAU - Temme, A
AU  - Temme A
AD  - Institut fur Genetik Abt. Molekulargenetik der Universitat Bonn, Romerstrasse 
      164, D-53117 Bonn, Germany. genetik@uni-bonn.de
FAU - Traub, O
AU  - Traub O
FAU - Willecke, K
AU  - Willecke K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Cell Tissue Res
JT  - Cell and tissue research
JID - 0417625
RN  - 0 (Albumins)
RN  - 0 (Connexins)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 127120-53-0 (Connexin 26)
RN  - 9001-32-5 (Fibrinogen)
SB  - IM
MH  - *Acute-Phase Reaction
MH  - Albumins/genetics
MH  - Animals
MH  - Blotting, Northern
MH  - Blotting, Western
MH  - Cell Communication/physiology
MH  - Cell Line, Transformed
MH  - Connexin 26
MH  - Connexins/*metabolism
MH  - Fibrinogen/genetics
MH  - Gap Junctions/*chemistry/metabolism
MH  - Gene Expression/drug effects
MH  - Interleukin-1/pharmacology
MH  - Interleukin-6/pharmacology
MH  - Liver/*chemistry/*cytology
MH  - Mice
MH  - RNA, Messenger/analysis
MH  - Transcription, Genetic/physiology
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Gap Junction beta-1 Protein
EDAT- 1998/11/03 00:00
MHDA- 1998/11/03 00:01
CRDT- 1998/11/03 00:00
PHST- 1998/11/03 00:00 [pubmed]
PHST- 1998/11/03 00:01 [medline]
PHST- 1998/11/03 00:00 [entrez]
AID - 10.1007/s004410051184 [doi]
PST - ppublish
SO  - Cell Tissue Res. 1998 Nov;294(2):345-50. doi: 10.1007/s004410051184.