Other formats:
BibTeX
LaTeX
RIS
@article{1336144,
author = {Sovadinová, Iva and Babica, Pavel and Boke, Hatice and Kumar, Esha and Wilke, Andrew and Park, JoonandSuk and Trosko, James E. and Upham, Brad L.},
article_location = {SAN FRANCISCO (USA)},
article_number = {5},
doi = {http://dx.doi.org/10.1371/journal.pone.0124454},
keywords = {Phosphatidylcholine; PLC-Induced Dysregulation; Gap Junctions; Environmental Toxicants; Rat Liver; Cell Model},
language = {eng},
issn = {1932-6203},
journal = {PLOS ONE},
title = {Phosphatidylcholine Specific PLC-Induced Dysregulation of Gap Junctions, a Robust Cellular Response to Environmental Toxicants, and Prevention by Resveratrol in a Rat Liver Cell Model},
url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124454#abstract0},
volume = {10},
year = {2015}
}
TY - JOUR
ID - 1336144
AU - Sovadinová, Iva - Babica, Pavel - Boke, Hatice - Kumar, Esha - Wilke, Andrew - Park, Joon-Suk - Trosko, James E. - Upham, Brad L.
PY - 2015
TI - Phosphatidylcholine Specific PLC-Induced Dysregulation of Gap Junctions, a Robust Cellular Response to Environmental Toxicants, and Prevention by Resveratrol in a Rat Liver Cell Model
JF - PLOS ONE
VL - 10
IS - 5
SP - "nestránkováno"
EP - "nestránkováno"
PB - Public Library of Science
SN - 19326203
KW - Phosphatidylcholine
KW - PLC-Induced Dysregulation
KW - Gap Junctions
KW - Environmental Toxicants
KW - Rat Liver
KW - Cell Model
UR - http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124454#abstract0
L2 - http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124454#abstract0
N2 - Dysregulation of gap junctional intercellular communication (GJIC) has been associated with different pathologies, including cancer; however, molecular mechanisms regulating GJIC are not fully understood. Mitogen Activated Protein Kinase (MAPK)-dependent mechanisms of GJIC-dysregulation have been well-established, recent discoveries have implicated phosphatidylcholine-specific phospholipase C (PC-PLC) in the regulation of GJIC. What is not known is how prevalent these two signaling mechanisms are in toxicant/toxin-induced dysregulation of GJIC, and do toxicants work through either signaling mechanisms or both. Different chemical toxicants were used to assess whether they dysregulate GJIC via MEK or PC-PLC, or both Mek and PC-PLC, or through other signaling pathways, using a pluripotent rat liver epithelial oval-cell line, WB-F344. Epidermal growth factor, 12-O-tetradecanoylphorbol-13-acetate, thrombin receptor activating peptide-6 and lindane regulated GJIC through a MEK1/2-dependent mechanism that was independent of PC-PLC; whereas PAHs, DDT, PCB 153, dicumylperoxide and perfluorodecanoic acid inhibited GJIC through PC-PLC independent of Mek. Resveratrol prevented dysregulation of GJIC by toxicants that acted either through MEK1/2 or PC-PLC. Except for alachlor, resveratrol did not prevent dysregulation of GJIC by toxicants that worked through PC-PLC-independent and MEK1/2-independent pathways. In conclusion: the dysregulation of GJIC is a contributing factor to the cancer process; however the underlying mechanisms by which gap junction channels are closed by toxicants vary. Thus, accurate assessments of risk posed by toxic agents, and the role of dietary phytochemicals play in preventing or reversing the effects of these agents must take into account the specific mechanisms involved in the cancer process.
ER -
SOVADINOVÁ, Iva, Pavel BABICA, Hatice BOKE, Esha KUMAR, Andrew WILKE, Joon-Suk PARK, James E. TROSKO and Brad L. UPHAM. Phosphatidylcholine Specific PLC-Induced Dysregulation of Gap Junctions, a Robust Cellular Response to Environmental Toxicants, and Prevention by Resveratrol in a Rat Liver Cell Model. \textit{PLOS ONE}. SAN FRANCISCO (USA): Public Library of Science, 2015, vol.~10, No~5, p.~''nestránkováno'', 16 pp. ISSN~1932-6203. Available from: https://dx.doi.org/10.1371/journal.pone.0124454.
|
