Please use this identifier to cite or link to this item:https://hdl.handle.net/20.500.12259/57964
Type of publication: research article
Type of publication (PDB): Straipsnis Clarivate Analytics Web of Science / Article in Clarivate Analytics Web of Science (S1)
Field of Science: Biologija / Biology (N010)
Author(s): Antanavičiūtė, Ieva;Mildažienė, Vida;Stankevičius, Edgaras;Herdegen, Thomas;Skeberdis, Vytenis Arvydas
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: p. 1-16
Date: 2014
Note: 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
Keywords: Connexin 43;Rabbit skeletal myoblasts;HeLa cells;Hyperthermia
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
Internet: http://downloads.hindawi.com/journals/mi/2014/748290.pdf
http://dx.doi.org/10.1155/2014/748290
Affiliation(s): Gamtos mokslų fakultetas
Kauno medicinos universiteto Kardiologijos institutas, arske@med.kmu.lt
Kauno medicinos universiteto Kardiologiojoas institutas
Lietuvos sveikatos mokslų universitetas
Lietuvos sveikatos mokslų universitetas, Kardiologijos institutas
Vytauto Didžiojo universitetas
Appears in Collections:Universiteto mokslo publikacijos / University Research Publications

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