Use this url to cite publication: https://hdl.handle.net/20.500.12259/57964
Publication type
type::text::periodical::journal::contribution to journal::journal article::research article
Type of publication (PDB)
Straipsnis Clarivate Analytics Web of Science / Article in Clarivate Analytics Web of Science (S1)
Author(s)
Kauno medicinos universiteto Kardiologiojoas institutas
Stankevičius, Edgaras
Lietuvos sveikatos mokslų universitetas
Herdegen, Thomas
Institute of experimental and clinical pharmacology, Kiel University
Skeberdis, Vytenis Arvydas
Kauno medicinos universiteto Kardiologijos institutas, arske@med.kmu.lt
Title
Hyperthermia differently affects Connexin43 expression and gap junction permeability in skeletal myoblasts and HeLa cells
Is part of
Mediators of inflammation. New York, NY : Hindawi Publishing Corporation, 2014, Vol. 2014
Extent
Publisher
New York, NY : Hindawi Publishing Corporation
Publisher (trusted)
Hindawi Publishing Corporation
Date Issued
2014
Description
Article ID 748290. IF 3,882. ISSN (electronic): 1466-1861. This work was supported by Lithuanian State Science and Studies Foundation Grant no. B-26/2007. The authors thank Professor Feliksas Bukauskas for providing HeLa cells expressing Cx43-EGFP
ISSN (of the container)
0962-9351
DOI
https://doi.org/10.1155/2014/748290
WOS
WOS:000340275500001
Other Identifier(s)
VDU02-000015654
Abstract
Stress kinases can be activated by hyperthermia and modify the expression level and properties of membranous and intercellular channels. We examined the role of c-Jun NH2-terminal kinase (JNK) in hyperthermia-induced changes of connexin43 (Cx43) expression and permeability of Cx43 gap junctions (GJs) in the rabbit skeletal myoblasts (SkMs) and Cx43-EGFP transfected HeLa cells. Hyperthermia (42°C for 6 h) enhanced the activity of JNK and its target, the transcription factor c-Jun, in both SkMs and HeLa cells. In SkMs, hyperthermia caused a 3.2-fold increase in the total Cx43 protein level and enhanced the efficacy of GJ intercellular communication (GJIC). In striking contrast, hyperthermia reduced the total amount of Cx43 protein, the number of Cx43 channels in GJ plaques, the density of hemichannels in the cell membranes, and the efficiency of GJIC in HeLa cells. Both in SkMs and HeLa cells, these changes could be prevented by XG-102, a JNK inhibitor. In HeLa cells, the changes in Cx43 expression and GJIC under hyperthermic conditions were accompanied by JNK-dependent disorganization of actin cytoskeleton stress fibers while in SkMs, the actin cytoskeleton remained intact. These findings provide an attractive model to identify the regulatory players within signalosomes, which determine the cell-dependent outcomes of hyperthermia.
Bibliographic Details
105
Coverage Spatial
US
Language
Anglų / English (en)