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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/50361
Title: Mitochondrial Dynamics Impairment in Dexamethasone-Treated Neuronal Cells
Authors: Wilasinee Suwanjang
Kay L.H. Wu
Supaluk Prachayasittikul
Banthit Chetsawang
Komgrid Charngkaew
Chang Gung Memorial Hospital
Mahidol University
Faculty of Medicine, Siriraj Hospital, Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Jan-2019
Citation: Neurochemical Research. (2019)
Abstract: © 2019, Springer Science+Business Media, LLC, part of Springer Nature. Dexamethasone is an approved steroid for clinical use to activate or suppress cytokines, chemokines, inflammatory enzymes and adhesion molecules. It enters the brain, by-passing the blood brain barrier, and acts through genomic mechanisms. High levels of dexamethasone are able to induce neuronal cell loss, reduce neurogenesis and cause neuronal dysfunction. The exact mechanisms of steroid, especially the dexamethasone contribute to neuronal damage remain unclear. Therefore, the present study explored the mitochondrial dynamics underlying dexamethasone-induced toxicity of human neuroblastoma SH-SY5Y cells. Neuronal cells treatment with the dexamethasone resulted in a marked decrease in cell proliferation. Dexamethasone-induced neurotoxicity also caused upregulation of mitochondrial fusion and cleaved caspase-3 proteins expression. Mitochondria fusion was found in large proportions of dexamethasone-treated cells. These results suggest that dexamethasone-induced hyperfused mitochondrial structures are associated with a caspase-dependent death process in dexamethasone-induced neurotoxicity. These findings point to the high dosage of dexamethasone as being neurotoxic through impairment of mitochondrial dynamics.
URI: http://repository.li.mahidol.ac.th/dspace/handle/123456789/50361
metadata.dc.identifier.url: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85063087527&origin=inward
ISSN: 15736903
03643190
Appears in Collections:Scopus 2019

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