Matches in SemOpenAlex for { <https://semopenalex.org/work/W2890634550> ?p ?o ?g. }
- W2890634550 abstract "Autoimmune rheumatic lesions are often characterised by the immune cell recruitment including B lymphocytes and the presence of reactive oxygen species (ROS), which increase antioxidant gene transcription via nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Spleen tyrosine kinase (Syk) has a major role in the signal transmission of all haematopoietic lineage cells including B/T cells, mast cells, and macrophages. In this study, we investigated whether B cell survival is regulated by Nrf2 via ROS-mediated Syk activation in WiL2-NS human B lymphoblast cells. When WiL2-NS cells were incubated with 1% foetal bovine serum (FBS), the survival rate and mitochondrial membrane potential (MMP) were reduced. In addition, 1% FBS increased caspase 3 activity, cytochrome C release, nuclear localisation of Nrf2, and ROS production. N-acetylcysteine attenuated ROS production and nuclear translocation of Nrf2. It also inhibited cell death, caspase 3 activation, MMP collapse, and cytochrome C release. Results from the 1% FBS treatment were consistent with those of H2O2 treatment. Syk phosphorylation at tyrosine 525/526 was increased by incubation with 1% FBS or treatment with 100 µM H2O2. Nuclear translocation of Nrf2 by H2O2 was inhibited by treatment with BAY61-3606, a Syk inhibitor. BAY61-3606 also promoted MMP collapse, cytochrome C release, caspase 3 activation, and cell death. Taken together, these results implicate that Syk controls oxidative stress-induced human B cell death via nuclear translocation of Nrf2 and MMP collapse. These results suggest that Syk is a novel regulator of Nrf2 activation." @default.
- W2890634550 created "2018-09-27" @default.
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- W2890634550 date "2018-09-02" @default.
- W2890634550 modified "2023-09-24" @default.
- W2890634550 title "Spleen tyrosine kinase-dependent Nrf2 activation regulates oxidative stress-induced cell death in WiL2-NS human B lymphoblasts" @default.
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- W2890634550 doi "https://doi.org/10.1080/10715762.2018.1505044" @default.
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