PMID- 10760574
OWN - NLM
STAT- MEDLINE
DCOM- 20000706
LR  - 20231213
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1491
IP  - 1-3
DP  - 2000 Apr 25
TI  - Liver cell-specific transcriptional regulation of connexin32.
PG  - 107-22
AB  - Gap junctional intercellular communication facilitates liver homeostasis and 
      growth control in the liver. The major gap junction protein expressed by 
      hepatocytes is connexin32 (Cx32) and non-parenchymal hepatic cells do not express 
      this gene. We investigated the regulation of Cx32 transcription by 
      trans-activating factors in liver cells. Transient transfection assays using 
      deletions of the rat Cx32 promoter (nt -753 to -33) linked to the luciferase gene 
      were performed in MH1C1 rat hepatoma cells that express endogenous Cx32 compared 
      with WB-F344 rat liver epithelial cells that do not. The basal promoter element 
      was located within nt -134 to -33 and was 1.4-fold more active in MH1C1 cells 
      than WB-F344 cells whereas the entire promoter fragment (nt -754 to -33) was 
      four-fold more active in MH1C1 cells. Specific nuclear protein-DNA complexes that 
      bound to Sp1 consensus sites within the basal promoter were formed using nuclear 
      extracts from both types of cells. Additional promoter sequences increased 
      promoter activity more strongly in MH1C1 cells than WB-F344 cells and this was 
      correlated with the binding of hepatocyte nuclear factor-1 (HNF-1) to two HNF-1 
      consensus sites centered at -187 and -736. Expression of HNF-1 and binding to 
      these elements was only observed with MH1C1 cells. Other specific protein-DNA 
      complexes were formed, however, that included YY-1- and NF-1-containing 
      complexes, but these were not related to promoter activity. Dexamethasone 
      increased Cx32 promoter activity and expression in MH1C1 cells, but had little 
      effect in WB-F344 cells and did not alter protein-DNA complex formation. These 
      data suggest that Sp1 is responsible for Cx32 promoter basal activity, that HNF-1 
      determines the cell-specific expression of Cx32, and that dexamethasone increases 
      Cx32 expression through other mechanisms.
FAU - Piechocki, M P
AU  - Piechocki MP
AD  - Department of Pathology, Medical College of Ohio, 3055 Arlington Avenue, Toledo, 
      OH, USA.
FAU - Toti, R M
AU  - Toti RM
FAU - Fernstrom, M J
AU  - Fernstrom MJ
FAU - Burk, R D
AU  - Burk RD
FAU - Ruch, R J
AU  - Ruch RJ
LA  - eng
GR  - CA-R29-57612/CA/NCI NIH HHS/United States
GR  - DK-5P30-41296/DK/NIDDK NIH HHS/United States
GR  - DK-PO1-41918/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Connexin 43)
RN  - 0 (Connexins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Hepatocyte Nuclear Factor 1-alpha)
RN  - 0 (Hnf1a protein, rat)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Transcription Factors)
RN  - 126548-29-6 (Hepatocyte Nuclear Factor 1)
RN  - 138674-15-4 (Hepatocyte Nuclear Factor 1-beta)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Binding Sites
MH  - Connexin 43/genetics/metabolism
MH  - Connexins/*genetics/metabolism
MH  - *DNA-Binding Proteins
MH  - Dexamethasone/pharmacology
MH  - Gene Expression Regulation
MH  - Hepatocyte Nuclear Factor 1
MH  - Hepatocyte Nuclear Factor 1-alpha
MH  - Hepatocyte Nuclear Factor 1-beta
MH  - Liver/*metabolism
MH  - Molecular Sequence Data
MH  - Nuclear Proteins/metabolism
MH  - Promoter Regions, Genetic
MH  - Rats
MH  - Sequence Deletion
MH  - Transcription Factors/metabolism
MH  - Transcription, Genetic
MH  - Transfection
MH  - Tumor Cells, Cultured
MH  - Gap Junction beta-1 Protein
EDAT- 2000/04/13 09:00
MHDA- 2000/07/08 11:00
CRDT- 2000/04/13 09:00
PHST- 2000/04/13 09:00 [pubmed]
PHST- 2000/07/08 11:00 [medline]
PHST- 2000/04/13 09:00 [entrez]
AID - S0167-4781(00)00036-1 [pii]
AID - 10.1016/s0167-4781(00)00036-1 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2000 Apr 25;1491(1-3):107-22. doi: 
      10.1016/s0167-4781(00)00036-1.