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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F15%3A00086654" target="_blank" >RIV/00216224:14310/15:00086654 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/67985939:_____/15:00448049

Výsledek na webu

<a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124454#abstract0" target="_blank" >http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0124454#abstract0</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1371/journal.pone.0124454" target="_blank" >10.1371/journal.pone.0124454</a>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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)-dependentmechanisms 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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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)-dependentmechanisms 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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

DN - Vliv životního prostředí na zdraví

OECD FORD obor

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Projekt

<a href="/cs/project/LH12034" target="_blank" >LH12034: Nový in vitro přístup pro identifikaci chemopreventivních účinků a mechanismů fytochemikálií</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

PLOS ONE

ISSN

1932-6203

e-ISSN

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Svazek periodika

10

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

16

Strana od-do

"nestránkováno"

Kód UT WoS článku

000355319400005

EID výsledku v databázi Scopus

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