Mitochondrial-Targeted Antioxidant MitoQ Prevents E. coli Lipopolysaccharide-Induced Accumulation of Triacylglycerol and Lipid Droplets Biogenesis in Epithelial Cells

Autor:	E. M. Fock, Rimma G. Parnova, Vera Bachteeva, Lavrova Ea
Jazyk:	angličtina
Rok vydání:	2018
Předmět:	0301 basic medicine chemistry.chemical_classification Mitochondrial ROS MitoQ Article Subject Lipopolysaccharide lcsh:QP1-981 Cellular respiration Fatty acid Mitochondrion Biochemistry lcsh:Physiology Cell biology lcsh:Biochemistry 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology chemistry Lipid droplet lcsh:QD415-436 Intracellular
Zdroj:	Journal of Lipids, Vol 2018 (2018)
ISSN:	2090-3049 2090-3030
Popis:	The effect of bacterial lipopolysaccharide (LPS) on eukaryotic cell could be accompanied by a significant metabolic shift that includes accumulation of triacylglycerol (TAG) in lipid droplets (LD), ubiquitous organelles associated with fatty acid storage, energy regulation and demonstrated tight spatial and functional connections with mitochondria. The impairment of mitochondrial activity under pathological stimuli has been shown to provoke TAG storage and LD biogenesis. However the potential mechanisms that link mitochondrial disturbances and TAG accumulation are not completely understood. We hypothesize that mitochondrial ROS (mROS) may play a role of a trigger leading to subsequent accumulation of intracellular TAG and LD in response to a bacterial stimulus. Using isolated epithelial cells from the frog urinary bladder, we showed that LPS decreased fatty acids oxidation, enhanced TAG deposition, and promoted LD formation. LPS treatment did not affect the mitochondrial membrane potential but increased cellular ROS production and led to impairment of mitochondrial function as revealed by decreased ATP production and a reduced maximal oxygen consumption rate (OCR) and OCR directed at ATP turnover. The mitochondrial-targeted antioxidant MitoQ at a dose of 25 nM did not prevent LPS-induced alterations in cellular respiration, but, in contrast to nonmitochondrial antioxidant α-tocopherol, reduced the effect of LPS on the generation of ROS, restored the LPS-induced decline of fatty acids oxidation, and prevented accumulation of TAG and LD biogenesis. The data obtained indicate the key signaling role of mROS in the lipid metabolic shift that occurs under the impact of a bacterial pathogen in epithelial cells.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4a5161de77a7668208246b1f31616144 https://doaj.org/article/0ecde5ddb9214530be558cd288b27f3e Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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