flow-cytometric-analysis-lymphocyte-infiltration-central-nervous

Flow Cytometric Analysis of Lymphocyte Infiltration in Central Nervous System during Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) caused by the combination of environmental factors and susceptible ...

global-current-research-trends-single-cell-sequencing-cancer

Global and Current Research Trends of Single-Cell Sequencing in Cancer: A Bibliometric and Visualization Study

Cancer poses a significant challenge to human health due to its complex biological systems, necessitating in-depth analysis. Single-cell sequencing has ...

Shanghai Jiao Tong University School of Medicine

Tongji University School of Medicine

Tianjin Medical University General Hospital, Tianjin Medical University

Heavy alcohol exposure causes profound damage to the adolescent brain, particularly the hippocampus, which underlie some behavioral deficits. However, the underlying molecular mechanisms remain inconclusive. The current study sought to determine whether binge alcohol exposure affects the hippocampus-related behaviors and key signaling proteins that may mediate alcohol neurotoxicity in adolescent rats. Alcohol exposure reduced the number of both NeuN-positive and doublecortin-positive cells in the hippocampus. Alcohol also induced neurodegeneration which was confirmed by ultrastructural analysis by electronic microscopy and was accompanied with the activation of microglia. Binge alcohol exposure impaired spatial learning and memory which was evaluated by the Morris water maze. However, alcohol did not alter the spontaneous locomotor activity which was determined by the open field test. GSK3β is a multi-function serine/threonine protein kinase regulating both neuronal survival and neurogenesis and plays an important role in various neurodegenerative disorders. We have previously shown that GSK3β is a key mediator of alcohol-induced neuron apoptosis in the developing brain. We showed here binge alcohol exposure caused GSK3β activation by inducing dephosphorylation at Ser9 without affecting the phosphorylation of Tyr216 in the hippocampus. Thus, GSK3β may be involved in binge alcohol exposure-induced neuronal damage to the adolescent hippocampus.

Binge Alcohol Exposure Causes Neurobehavioral Deficits and GSK3β Activation in the Hippocampus of Adolescent Rats.

Growing evidence suggests that obesity is associated with the susceptibility and disease severity of multiple sclerosis. The chronic inflammation induced by obesity is believed to contribute to this process. However, the immune mechanisms connecting obesity to the prevalence and pathogenesis of MS are poorly defined. In this study, we show that high fat diet (HFD)-induced obese mice developed an exacerbated EAE as indicated by higher clinical scores and more severe pathological changes in spinal cord than the control mice fed with normal diet (ND), following immunization with myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide. The exacerbation of EAE in HFD mice was associated with enhanced microglial activation and increased expansion of Th1 and Th17 cells. The HFD mice also showed aggravated disease in an adoptive T cell transfer EAE model. Mechanistically, HFD augmented the expression level of IL-6 and CCL-2 both in serum and brain, and blockade of IL-6 and CCL-2 signal ameliorated EAE with reduced T cells infiltration in CNS. Taken together, our results suggest that obesity promotes CNS inflammation in EAE through IL-6 and CCL-2 mediated the inflammatory cells infiltration.

ArticleTotal : 2	Year
Publication title Cited by 1	2020
Publication title	2025

Article	Year
Binge Alcohol Exposure Causes Neurobehavioral Deficits and GSK3β Activation in the Hippocampus of Adolescent Rats. Scientific reports\| PubMed ID: 29449568	2018
Obesity Promotes EAE Through IL-6 and CCL-2-Mediated T Cells Infiltration. Frontiers in immunology\| PubMed ID: 31507583	2019

Zhe Ji

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