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Transfer of IP3 through gap junctions is critical, but not sufficient, for the spread of apoptosis

Elke Decrock UGent, Dmitri Krysko UGent, Mathieu Vinken, Agnieszka Kaczmarek UGent, Giulia Crispino, MELISSA BOL UGent, Nan Wang UGent, Marijke De Bock UGent, Elke De Vuyst UGent and Christian C Naus, et al. (2012) CELL DEATH AND DIFFERENTIATION. 19(6). p.947-957
abstract
Decades of research have indicated that gap junction channels contribute to the propagation of apoptosis between neighboring cells. Inositol 1,4,5-trisphosphate (IP3) has been proposed as the responsible molecule conveying the apoptotic message, although conclusive results are still missing. We investigated the role of IP3 in a model of gap junction-mediated spreading of cytochrome C-induced apoptosis. We used targeted loading of high-molecular-weight agents interfering with the IP3 signaling cascade in the apoptosis trigger zone and cell death communication zone of C6-glioma cells heterologously expressing connexin (Cx)43 or Cx26. Blocking IP3 receptors or stimulating IP3 degradation both diminished the propagation of apoptosis. Apoptosis spread was also reduced in cells expressing mutant Cx26, which forms gap junctions with an impaired IP3 permeability. However, IP3 by itself was not able to induce cell death, but only potentiated cell death propagation when the apoptosis trigger was applied. We conclude that IP3 is a key necessary messenger for communicating apoptotic cell death via gap junctions, but needs to team up with other factors to become a fully pro-apoptotic messenger.
Please use this url to cite or link to this publication:
author
organization
alternative title
Transfer of IP(3) through gap junctions is critical, but not sufficient, for the spread of apoptosis
year
type
journalArticle (original)
publication status
published
subject
keyword
CA2+, BH4 DOMAIN, 1, 4, 5-TRISPHOSPHATE, BAX, PERMEABILITY, CALCIUM-RELEASE, ENDOPLASMIC-RETICULUM, CYTOCHROME-C, INOSITOL TRISPHOSPHATE RECEPTOR, CELL-DEATH, gap junction, 5-trisphosphate, apoptosis, calcium, connexin, inositol 1
journal title
CELL DEATH AND DIFFERENTIATION
Cell Death Differ.
volume
19
issue
6
pages
947 - 957
Web of Science type
Article
Web of Science id
000303822800005
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
8.371 (2012)
JCR rank
26/288 (2012)
JCR quartile
1 (2012)
ISSN
1350-9047
DOI
10.1038/cdd.2011.176
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2106480
handle
http://hdl.handle.net/1854/LU-2106480
date created
2012-05-14 21:45:29
date last changed
2012-06-13 13:48:46
@article{2106480,
  abstract     = {Decades of research have indicated that gap junction channels contribute to the propagation of apoptosis between neighboring cells. Inositol 1,4,5-trisphosphate (IP3) has been proposed as the responsible molecule conveying the apoptotic message, although conclusive results are still missing. We investigated the role of IP3 in a model of gap junction-mediated spreading of cytochrome C-induced apoptosis. We used targeted loading of high-molecular-weight agents interfering with the IP3 signaling cascade in the apoptosis trigger zone and cell death communication zone of C6-glioma cells heterologously expressing connexin (Cx)43 or Cx26. Blocking IP3 receptors or stimulating IP3 degradation both diminished the propagation of apoptosis. Apoptosis spread was also reduced in cells expressing mutant Cx26, which forms gap junctions with an impaired IP3 permeability. However, IP3 by itself was not able to induce cell death, but only potentiated cell death propagation when the apoptosis trigger was applied. We conclude that IP3 is a key necessary messenger for communicating apoptotic cell death via gap junctions, but needs to team up with other factors to become a fully pro-apoptotic messenger.},
  author       = {Decrock, Elke and Krysko, Dmitri and Vinken, Mathieu and Kaczmarek, Agnieszka and Crispino, Giulia and BOL, MELISSA and Wang, Nan and De Bock, Marijke and De Vuyst, Elke and Naus, Christian C and Rogiers, Vera and Vandenabeele, Peter and Erneux, Christophe and Mammano, Fabio and Bultynck, Geert and Leybaert, Luc},
  issn         = {1350-9047},
  journal      = {CELL DEATH AND DIFFERENTIATION},
  keyword      = {CA2+,BH4 DOMAIN,1,4,5-TRISPHOSPHATE,BAX,PERMEABILITY,CALCIUM-RELEASE,ENDOPLASMIC-RETICULUM,CYTOCHROME-C,INOSITOL TRISPHOSPHATE RECEPTOR,CELL-DEATH,gap junction,5-trisphosphate,apoptosis,calcium,connexin,inositol 1},
  language     = {eng},
  number       = {6},
  pages        = {947--957},
  title        = {Transfer of IP3 through gap junctions is critical, but not sufficient, for the spread of apoptosis},
  url          = {http://dx.doi.org/10.1038/cdd.2011.176},
  volume       = {19},
  year         = {2012},
}

Chicago
Decrock, Elke, Dmitri Krysko, Mathieu Vinken, Agnieszka Kaczmarek, Giulia Crispino, Mélissa Bol, Nan Wang, et al. 2012. “Transfer of IP3 Through Gap Junctions Is Critical, but Not Sufficient, for the Spread of Apoptosis.” Cell Death and Differentiation 19 (6): 947–957.
APA
Decrock, E., Krysko, D., Vinken, M., Kaczmarek, A., Crispino, G., Bol, M., Wang, N., et al. (2012). Transfer of IP3 through gap junctions is critical, but not sufficient, for the spread of apoptosis. CELL DEATH AND DIFFERENTIATION, 19(6), 947–957.
Vancouver
1.
Decrock E, Krysko D, Vinken M, Kaczmarek A, Crispino G, Bol M, et al. Transfer of IP3 through gap junctions is critical, but not sufficient, for the spread of apoptosis. CELL DEATH AND DIFFERENTIATION. 2012;19(6):947–57.
MLA
Decrock, Elke, Dmitri Krysko, Mathieu Vinken, et al. “Transfer of IP3 Through Gap Junctions Is Critical, but Not Sufficient, for the Spread of Apoptosis.” CELL DEATH AND DIFFERENTIATION 19.6 (2012): 947–957. Print.