ArticleJournal of cellular and molecular medicine2015
A novel TXNIP-based mechanism for Cx43-mediated regulation of oxidative drug injury.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- A myeloid leukemia factor homolog is involved in tolerance to stresses and stress-induced protein metabolism in Giardia lamblia.Biology direct · 2023Article
- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Bioglass promotes wound healing by inhibiting endothelial cell pyroptosis through regulation of the connexin 43/reactive oxygen species (ROS) signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- A Novel Multiprotein Bridging Factor 1-Like Protein Induces Cyst Wall Protein Gene Expression and Cyst Differentiation inInternational journal of molecular sciences · 2021Article
- Glycyrrhetinic Acid Protects Renal Tubular Cells against Oxidative Injury via Reciprocal Regulation of JNK-Connexin 43-Thioredoxin 1 Signaling.Frontiers in pharmacology · 2021Article
- Gap junctions amplify TRPV4 activation-initiated cell injury via modification of intracellular CaChannels (Austin, Tex.) · 2020Article
- DNA topoisomerase IIIβ promotes cyst generation by inducing cyst wall protein gene expression inOpen biology · 2020Article
- Connexin43 Is Required for the Effective Activation of Spleen Cells and Immunoglobulin Production.International journal of molecular sciences · 2019Article
- Scutellarin protects oxygen/glucose-deprived astrocytes and reduces focal cerebral ischemic injury.Neural regeneration research · 2018Article
- Antipsychotic inductors of brain hypothermia and torpor-like states: perspectives of application.Psychopharmacology · 2017Review
- Heterozygous connexin 50 mutation affects metabolic syndrome attributes in spontaneously hypertensive rat.Lipids in health and disease · 2016Article
- Connexin43 hemichannels contributes to the disassembly of cell junctions through modulation of intracellular oxidative status.Redox biology · 2016Article
- Upregulation of connexin43 contributes to PX-12-induced oxidative cell death.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- TXNIP/TRX/NF-κB and MAPK/NF-κB pathways involved in the cardiotoxicity induced by Venenum Bufonis in rats.Scientific reports · 2016Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gap junctions (GJs) play an important role in the regulation of cell response to many drugs. However, little is known about their mechanisms. Using an in vitro model of cytotoxicity induced by geneticin (G418), we explored the potential signalling mechanisms involved. Incubation of cells with G418 resulted in cell death, as indicated by the change in cell morphology, loss of cell viability and activation of caspase-3. Before the onset of cell injury, G418 induced reactive oxygen species (ROS) generation, activated oxidative sensitive kinase P38 and caused a shift of connexin 43 (Cx43) from non-phosphorylated form to hyperphosphorylated form. These changes were largely prevented by antioxidants, suggesting an implication of oxidative stress. Downregulation of Cx43 with inhibitors or siRNA suppressed the expression of thioredoxin-interacting protein (TXNIP), activated Akt and protected cells against the toxicity of G418. Further analysis revealed that inhibition of TXNIP with siRNA activated Akt and reproduced the protective effect of Cx43-inhibiting agents, whereas suppression of Akt sensitized cells to the toxicity of G418. Furthermore, interference of TXNIP/Akt also affected puromycin- and adriamycin-induced cell injury. Our study thus characterized TXNIP as a presently unrecognized molecule implicated in the regulatory actions of Cx43 on oxidative drug injury. Targeting Cx43/TXNIP/Akt signalling cascade might be a promising approach to modulate cell response to drugs.
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