TNFR2 mediated neuroprotection via PI3K/NF-κB pathway 1 TNF mediated neuroprotection against glutamate induced excitotoxicity is enhanced by NMDA receptor activation: Essential role of a TNF receptor 2 mediated, PI3 kinase dependent NF-κB pathway
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Reactive oxygen species mediate TNF-α-induced inflammatory response in bone marrow mesenchymal cells
Objective(s): It is generally believed that the inflammatory response in bone marrow mesenchymal stem cells (BMSCs) transplantation leads to poor survival and unsatisfactory effects, and is mainly mediated by cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α). In this study, we explored the mechanisms underlying the TNF-α-induced inflammatory ...
متن کاملBoth internalization and AIP1 association are required for tumor necrosis factor receptor 2-mediated JNK signaling.
OBJECTIVE The proinflammtory cytokine tumor necrosis factor (TNF), primarily via TNF receptor 1 (TNFR1), induces nuclear factor-κB (NF-κB)-dependent cell survival, and c-Jun N-terminal kinase (JNK) and caspase-dependent cell death, regulating vascular endothelial cell (EC) activation and apoptosis. However, signaling by the second receptor, TNFR2, is poorly understood. The goal of this study wa...
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Statins are widely used as medication to lower cholesterol levels in human patients. In addition, it was recently reported that they also reduce the incidence of stroke and progression of Alzheimer's disease when prophylactically administered. To date there is only limited information available on how statins exert this beneficial effect. In this study we investigated the neuroprotective effect...
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Glutamate-mediated excitotoxicity and neurodegeneration have been shown as pathophysiological hallmarks of multiple sclerosis (MS) and other autoimmune inflammatory CNS disorders. N‑Methyl‑D‑Aspartate (NMDA) receptors play a pivotal role in the mediation of neuronal glutamate excitotoxicity leading to cellular damage and apoptotic cell death. Current treatment approaches targeting glutamate exc...
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