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Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death

Mathieu Vinken, Elke Decrock UGent, Elke De Vuyst UGent, Marijke De Bock UGent, Roosmarijn Vandenbroucke UGent, Bruno De Geest UGent, Jo Demeester UGent, Niek Sanders UGent, Tamara Vanhaecke and Luc Leybaert UGent, et al. (2010) CELLULAR AND MOLECULAR LIFE SCIENCES. 67(6). p.907-918
abstract
The present study was set up to investigate the fate of connexin32 and its channels in hepatocellular apoptosis. Primary hepatocyte cultures were exposed to Fas ligand and cycloheximide, and modifications in connexin32 expression and localization, and gap junction functionality were studied. We found that gap junction functionality rapidly declined upon progression of cell death, which was associated with a decay of the gap junctional connexin32 protein pool. Simultaneously, levels of newly synthesized connexin32 protein increased and gathered in a hemichannel configuration. This became particularly evident towards the end stages of the cell death process and was not reflected at the transcriptional level. We next either silenced connexin32 expression or inhibited connexin32 hemichannel activity prior to cell death induction. Both approaches resulted in a delayed termination of the cell death response. We conclude that connexin32 hemichannels facilitate the apoptotic-to-necrotic transition, which typically occurs in the final stage of hepatocellular apoptosis.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
Primary hepatocyte, Gap junction, Apoptosis, Connexin32, Hemichannel, GAP-JUNCTION CHANNELS, RAT HEPATOCYTES, ACTIVATED MICROGLIA, PRIMARY CULTURE, IDENTIFICATION, TRICHOSTATIN, PROPAGATION, SURVIVAL, NECROSIS, RELEASE
journal title
CELLULAR AND MOLECULAR LIFE SCIENCES
Cell. mol. life sci.
volume
67
issue
6
pages
907 - 918
Web of Science type
Review
Web of Science id
000274903200005
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
7.047 (2010)
JCR rank
35/284 (2010)
JCR quartile
1 (2010)
ISSN
1420-682X
DOI
10.1007/s00018-009-0220-2
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
805294
handle
http://hdl.handle.net/1854/LU-805294
date created
2009-12-09 12:54:50
date last changed
2012-06-26 14:31:56
@article{805294,
  abstract     = {The present study was set up to investigate the fate of connexin32 and its channels in hepatocellular apoptosis. Primary hepatocyte cultures were exposed to Fas ligand and cycloheximide, and modifications in connexin32 expression and localization, and gap junction functionality were studied. We found that gap junction functionality rapidly declined upon progression of cell death, which was associated with a decay of the gap junctional connexin32 protein pool. Simultaneously, levels of newly synthesized connexin32 protein increased and gathered in a hemichannel configuration. This became particularly evident towards the end stages of the cell death process and was not reflected at the transcriptional level. We next either silenced connexin32 expression or inhibited connexin32 hemichannel activity prior to cell death induction. Both approaches resulted in a delayed termination of the cell death response. We conclude that connexin32 hemichannels facilitate the apoptotic-to-necrotic transition, which typically occurs in the final stage of hepatocellular apoptosis.},
  author       = {Vinken, Mathieu and Decrock, Elke and De Vuyst, Elke and De Bock, Marijke and Vandenbroucke, Roosmarijn and De Geest, Bruno and Demeester, Jo and Sanders, Niek and Vanhaecke, Tamara and Leybaert, Luc and Rogiers, Vera},
  issn         = {1420-682X},
  journal      = {CELLULAR AND MOLECULAR LIFE SCIENCES},
  keyword      = {Primary hepatocyte,Gap junction,Apoptosis,Connexin32,Hemichannel,GAP-JUNCTION CHANNELS,RAT HEPATOCYTES,ACTIVATED MICROGLIA,PRIMARY CULTURE,IDENTIFICATION,TRICHOSTATIN,PROPAGATION,SURVIVAL,NECROSIS,RELEASE},
  language     = {eng},
  number       = {6},
  pages        = {907--918},
  title        = {Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death},
  url          = {http://dx.doi.org/10.1007/s00018-009-0220-2},
  volume       = {67},
  year         = {2010},
}

Chicago
Vinken, Mathieu, Elke Decrock, Elke De Vuyst, Marijke De Bock, Roosmarijn Vandenbroucke, Bruno De Geest, Jo Demeester, et al. 2010. “Connexin32 Hemichannels Contribute to the Apoptotic-to-necrotic Transition During Fas-mediated Hepatocyte Cell Death.” Cellular and Molecular Life Sciences 67 (6): 907–918.
APA
Vinken, M., Decrock, E., De Vuyst, E., De Bock, M., Vandenbroucke, R., De Geest, B., Demeester, J., et al. (2010). Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death. CELLULAR AND MOLECULAR LIFE SCIENCES, 67(6), 907–918.
Vancouver
1.
Vinken M, Decrock E, De Vuyst E, De Bock M, Vandenbroucke R, De Geest B, et al. Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death. CELLULAR AND MOLECULAR LIFE SCIENCES. 2010;67(6):907–18.
MLA
Vinken, Mathieu, Elke Decrock, Elke De Vuyst, et al. “Connexin32 Hemichannels Contribute to the Apoptotic-to-necrotic Transition During Fas-mediated Hepatocyte Cell Death.” CELLULAR AND MOLECULAR LIFE SCIENCES 67.6 (2010): 907–918. Print.