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- W2249603670 abstract "Dendritic cells (DCs), antigen-presenting cells critically important for primary immune response and establishment of immunological memory, are activated by bacterial lipopolysaccharides (LPS) resulting in stimulation of Na(+)/H(+) exchanger, ROS formation and migration. The effects are dependent on phosphoinositide 3 (PI3) kinase and paralleled by Akt phosphorylation. The present study explored the contribution of the Akt isoform Akt1.Cytosolic pH (pH(i)) (2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein [BCECF] fluorescence), Na(+)/H(+) exchanger activity (Na(+) dependent realkalinization after an ammonium pulse), cell volume (forward scatter in FACS analysis), and ROS production (2',7'-dichlorodihydrofluorescein diacetate [DCFDA] fluorescence) were determined in DCs isolated from bone marrow of mice lacking functional Akt1/PKBα (akt1(-/-)) and their wild type littermates (akt1(+/+)).Forward scatter was lower in akt1(-/-) than in akt1(+/+) DCs, whereas pH(i), Na(+)/H(+) exchanger activity and ROS formation were less in untreated akt1(-/-) and akt1(+/+) DCs. Exposure of DCs to LPS was followed by increase of forward scatter and ROS formation to a similar extent in akt1(-/-) and in akt1(+/+) DCs. A 4 hours treatment with either LPS (1µg/ml) or tert-butylhydroperoxide (tBOOH, 5 µM) significantly stimulated Na(+)/H(+) exchanger activity in both genotypes, effects, however, significantly blunted in akt1(-/-) DCs.The present observations demonstrate that Akt1 is required for the full stimulation of Na(+)/H(+) exchanger activity by LPS or oxidative stress in dendritic cells." @default.
- W2249603670 created "2016-06-24" @default.
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- W2249603670 date "2015-01-01" @default.
- W2249603670 modified "2023-10-18" @default.
- W2249603670 title "Regulation of Na+/H+ Exchanger in Dendritic Cells by Akt1" @default.
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- W2249603670 doi "https://doi.org/10.1159/000430293" @default.
- W2249603670 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26138884" @default.
- W2249603670 hasPublicationYear "2015" @default.
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