Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells

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...

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Main Authors: Ieva Antanavičiūtė, Vida Mildažienė, Edgaras Stankevičius, Thomas Herdegen, Vytenis Arvydas Skeberdis
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/748290
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author Ieva Antanavičiūtė
Vida Mildažienė
Edgaras Stankevičius
Thomas Herdegen
Vytenis Arvydas Skeberdis
author_facet Ieva Antanavičiūtė
Vida Mildažienė
Edgaras Stankevičius
Thomas Herdegen
Vytenis Arvydas Skeberdis
author_sort Ieva Antanavičiūtė
collection DOAJ
description 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.
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spelling doaj-art-2a54d1d8597e4a3daaea71d64b6534562025-08-20T03:54:37ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/748290748290Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa CellsIeva Antanavičiūtė0Vida Mildažienė1Edgaras Stankevičius2Thomas Herdegen3Vytenis Arvydas Skeberdis4Institute of Cardiology, Lithuanian University of Health Sciences, Sukilėlių Avenue 17, 50009 Kaunas, LithuaniaInstitute of Cardiology, Lithuanian University of Health Sciences, Sukilėlių Avenue 17, 50009 Kaunas, LithuaniaInstitute of Physiology and Pharmacology, Lithuanian University of Health Sciences, 44307 Kaunas, LithuaniaInstitute of Experimental and Clinical Pharmacology, Kiel University, Hospitalstraße 4, 24105 Kiel, GermanyInstitute of Cardiology, Lithuanian University of Health Sciences, Sukilėlių Avenue 17, 50009 Kaunas, LithuaniaStress 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.http://dx.doi.org/10.1155/2014/748290
spellingShingle Ieva Antanavičiūtė
Vida Mildažienė
Edgaras Stankevičius
Thomas Herdegen
Vytenis Arvydas Skeberdis
Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells
Mediators of Inflammation
title Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells
title_full Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells
title_fullStr Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells
title_full_unstemmed Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells
title_short Hyperthermia Differently Affects Connexin43 Expression and Gap Junction Permeability in Skeletal Myoblasts and HeLa Cells
title_sort hyperthermia differently affects connexin43 expression and gap junction permeability in skeletal myoblasts and hela cells
url http://dx.doi.org/10.1155/2014/748290
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