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

0448049 - BÚ 2016 RIV US eng J - Journal Article
Sovadinová, I. - Babica, Pavel - Böke, H. - Kumar, E. - Wilke, A. - Park, J.-S. - Trosko, J. E. - Upham, B. L.
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.
PLoS ONE. Roč. 10, 5 no.e0124454 (2015), s. 1-16. ISSN 1932-6203. E-ISSN 1932-6203
R&D Projects: GA MŠMT LH12034
Institutional support: RVO:67985939
Keywords : gap junctional intercellular communication * resveratrol * phosphatidylcholine-specific phospholipase C
Subject RIV: EB - Genetics ; Molecular Biology
Impact factor: 3.057, year: 2015

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, however 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/toxins work through either signaling mechanisms or both, or through alternative signaling mechanisms. 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.
Permanent Link: http://hdl.handle.net/11104/0249785