ArticleChinese neurosurgical journal2018
CD4 T cell deficiency attenuates ischemic stroke, inhibits oxidative stress, and enhances Akt/mTOR survival signaling pathways in mice.
Article in Chinese neurosurgical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- miR-542-3p attenuates corticosterone-induced hippocampal neuronal damage in depressive mice by modulating PTEN/AKT/GSK3β/β-catenin pathway.Biomolecules & biomedicine · 2025Article
- The impact of the let-7 family on the pathophysiological mechanisms of traumatic brain injury: a systematic review.Frontiers in neurology · 2025Review
- The efficacy of an allosteric modulator of the alpha 7 nicotinic acetylcholine receptor in a murine model of stroke.Frontiers in neuroscience · 2025Article
- Article
- Targeting foam cell formation to improve recovery from ischemic stroke.Neurobiology of disease · 2023Review
- Control of the temporal development of Alzheimer's disease pathology by the MR1/MAIT cell axis.Journal of neuroinflammation · 2023Article
- Modulation of mTOR Signaling in Cardiovascular Disease to Target Acute and Chronic Inflammation.Frontiers in cardiovascular medicine · 2022Review
- Review
- Baicalein, Baicalin, and Wogonin: Protective Effects against Ischemia-Induced Neurodegeneration in the Brain and Retina.Oxidative medicine and cellular longevity · 2021Review
- let-7g counteracts endothelial dysfunction and ameliorating neurological functions in mouse ischemia/reperfusion stroke model.Brain, behavior, and immunity · 2020Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundInhibition of CD4 T cells reduces stroke-induced infarction by inhibiting neuroinflammation in the ischemic brain in experimental stroke. Nevertheless, little is known about its effects on neuronal survival signaling pathways. In this study, we investigated the effects of CD4 T cell deficits on oxidative stress and on the Akt/mTOR cell signaling pathways after ischemic stroke in mice.
methodsMHC II gene knockout C57/BL6 mice, with significantly decreased CD4 T cells, were used. Stroke was induced by 60-min middle cerebral artery (MCA) occlusion. Ischemic brain tissues were harvested for Western blotting.
resultsThe impairment of CD4 T cell production resulted in smaller infarction. The Western blot results showed that iNOS protein levels robustly increased at 5 h and 24 h and then returned toward baseline at 48 h in wild-type mice after stroke, and gene KO inhibited iNOS at 5 h and 24 h. In contrast, the anti-inflammatory marker, arginase I, was found increased after stroke in WT mice, which was further enhanced in the KO mice. In addition, stroke resulted in increased phosphorylated PTEN, Akt, PRAS40, P70S6, and S6 protein levels in WT mice, which were further enhanced in the animals whose CD4 T cells were impaired.
conclusionThe impairment of CD4 T cell products prevents ischemic brain injury, inhibits inflammatory signals, and enhances the Akt/mTOR cell survival signaling pathways.
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