PMID- 20512937
OWN - NLM
STAT- MEDLINE
DCOM- 20100820
LR  - 20211020
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 110
IP  - 3
DP  - 2010 Jun 1
TI  - Enhanced connexin 43 expression delays intra-mitotic duration and cell cycle 
      traverse independently of gap junction channel function.
PG  - 772-82
LID - 10.1002/jcb.22590 [doi]
AB  - Connexins (Cxs) and gap junction (GJ)-mediated communication have been linked 
      with the regulation of cell cycle traverse. However, it is not clear whether Cx 
      expression or GJ channel function are the key mediators in this process or at 
      what stage this regulation may occur. We therefore tested the hypothesis that 
      enhanced Cx expression could alter the rate of cell cycle traverse independently 
      of GJ channel function. Sodium butyrate (NaBu) or anti-arrhythmic peptide (AAP10) 
      were used to enhance Cx expression in HeLa cells stably expressing Cx43 (HeLa-43) 
      and primary cultures of human fibroblasts (HFF) that predominantly express Cx43. 
      To reduce GJ-mediated communication, 18-alpha-glycyrrhetinic acid (GA) was used. 
      In HeLa-43 and HFF cells, NaBu and AAP10 enhanced Cx43 expression and increased 
      channel function, while GA reduced GJ-mediated communication but did not 
      significantly alter Cx43 expression levels. Timelapse microscopy and flow 
      cytometry of HeLa-WT (wild-type, Cx deficient) and HeLa-43 cells dissected cell 
      cycle traverse and enabled measurements of intra-mitotic time and determined 
      levels of G1 arrest. Enhanced Cx43 expression increased mitotic durations 
      corresponding with a G1 delay in cell cycle, which was linked to an increase in 
      expression of the cell cycle inhibitor p21(waf1/cip1) in both HeLa-43 and HFF 
      cells. Reductions in Cx43 channel function did not abrogate these responses, 
      indicating that GJ channel function was not a critical factor in reducing cell 
      proliferation in either cell type. We conclude that enhanced Cx43 expression and 
      not GJ-mediated communication, is involved in regulating cell cycle traverse.
CI  - (c) 2010 Wiley-Liss, Inc.
FAU - Johnstone, Scott R
AU  - Johnstone SR
AD  - Department of Biological and Biomedical Sciences, School of Life Sciences, 
      Glasgow Caledonian University, 70 Cowcaddens Rd, Glasgow, Scotland G4 0BA, UK.
FAU - Best, Angela K
AU  - Best AK
FAU - Wright, Catherine S
AU  - Wright CS
FAU - Isakson, Brant E
AU  - Isakson BE
FAU - Errington, Rachel J
AU  - Errington RJ
FAU - Martin, Patricia E
AU  - Martin PE
LA  - eng
GR  - R01 HL088554-05/HL/NHLBI NIH HHS/United States
GR  - CZB/606/04/CSO_/Chief Scientist Office/United Kingdom
GR  - R01 HL088554/HL/NHLBI NIH HHS/United States
GR  - BB/E012574/1/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - C23049/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom
GR  - R01088554/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Connexin 43)
SB  - IM
MH  - Blotting, Western
MH  - Cell Cycle/*physiology
MH  - Cell Separation
MH  - Connexin 43/*metabolism
MH  - Flow Cytometry
MH  - Fluorescent Antibody Technique
MH  - Gap Junctions/*physiology
MH  - HeLa Cells
MH  - Humans
MH  - Immunohistochemistry
MH  - Microscopy
MH  - Mitosis/*physiology
MH  - Time
PMC - PMC3030924
MID - NIHMS265619
COIS- The Authors have no conflict of interest to declare
EDAT- 2010/06/01 06:00
MHDA- 2010/08/21 06:00
PMCR- 2011/01/29
CRDT- 2010/06/01 06:00
PHST- 2010/06/01 06:00 [entrez]
PHST- 2010/06/01 06:00 [pubmed]
PHST- 2010/08/21 06:00 [medline]
PHST- 2011/01/29 00:00 [pmc-release]
AID - 10.1002/jcb.22590 [doi]
PST - ppublish
SO  - J Cell Biochem. 2010 Jun 1;110(3):772-82. doi: 10.1002/jcb.22590.