2015
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
SOVADINOVÁ, Iva, Pavel BABICA, Hatice BOKE, Esha KUMAR, Andrew WILKE et. al.Základní údaje
Originální název
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
Autoři
SOVADINOVÁ, Iva (203 Česká republika, domácí), Pavel BABICA (203 Česká republika), Hatice BOKE (840 Spojené státy), Esha KUMAR (840 Spojené státy), Andrew WILKE (840 Spojené státy), Joon-Suk PARK (840 Spojené státy), James E. TROSKO (840 Spojené státy) a Brad L. UPHAM (840 Spojené státy, garant)
Vydání
PLOS ONE, SAN FRANCISCO (USA), Public Library of Science, 2015, 1932-6203
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30304 Public and environmental health
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 3.057
Kód RIV
RIV/00216224:14310/15:00086654
Organizační jednotka
Přírodovědecká fakulta
UT WoS
000355319400005
Klíčová slova anglicky
Phosphatidylcholine; PLC-Induced Dysregulation; Gap Junctions; Environmental Toxicants; Rat Liver; Cell Model
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 8. 4. 2016 09:30, Ing. Andrea Mikešková
Anotace
V originále
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.