Global sphingosine-1-phosphate receptor 2 deficiency attenuates neuroinflammation and ischemic-reperfusion injury after neonatal stroke

Fukuzaki, Yumi; Faustino, Joel; Lecuyer, Matthieu; Rayasam, Aditya; Vexler, Zinaida S.

doi:10.1016/j.isci.2023.106340

Cited by 3 publications

(2 citation statements)

References 53 publications

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“…98 Global S1PR2 deletion enhances neuronal survival and attenuates both short-term and longer-term behavior deficits in a mouse PAIS model. 99 In neonatal rats, administration of a S1PR1/3/4/5, agonist FTY720 shortly after H-I is protective only in a combined model of LPS followed by H-I, but not following H-I alone, indicating that FTY720 affects the inflammatory injury component. JTE013, in turn, attenuates phosphorylation of MAP (mitogen-activated protein) kinases following LPS stimulation of BV2 cells and in postischemic brains 100 as well as suppresses LPS-triggered autophagy in primary microglia from S1P ablated mice.…”

Section: Lipid Signalingmentioning

confidence: 97%

Immune-Neurovascular Interactions in Experimental Perinatal and Childhood Arterial Ischemic Stroke

Mallard,

Ferriero,

Vexler

2024

Stroke

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Emerging clinical and preclinical data have demonstrated that the pathophysiology of arterial ischemic stroke in the adult, neonates, and children share similar mechanisms that regulate brain damage but also have distinct molecular signatures and involved cellular pathways due to the maturational stage of the central nervous system and the immune system at the time of the insult. In this review, we discuss similarities and differences identified thus far in rodent models of 2 different diseases—neonatal (perinatal) and childhood arterial ischemic stroke. In particular, we review acquired knowledge of the role of resident and peripheral immune populations in modulating outcomes in models of perinatal and childhood arterial ischemic stroke and the most recent and relevant findings in relation to the immune-neurovascular crosstalk, and how the influence of inflammatory mediators is dependent on specific brain maturation stages. Finally, we discuss the current state of treatments geared toward age-appropriate therapies that signal via the immune-neurovascular interaction and consider sex differences to achieve successful translation.

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Section: Lipid Signalingmentioning

confidence: 97%

Immune-Neurovascular Interactions in Experimental Perinatal and Childhood Arterial Ischemic Stroke

Mallard,

Ferriero,

Vexler

2024

Stroke

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“…Through phosphorylation, SRC activates various downstream immune response-related proteins, including retinoic acid-inducible gene 1 (RIG-1) protein, virus-induced signaling adapter (VISA) protein, stimulator of interferon gene protein (STING), TANK binding kinase 1 (TBK1) gene protein, and interferon regulatory factor 3 (IRF-3). Binding of sphingosine 1-phosphate receptor 2 by BAs can activate the extracellular signal-regulated kinase (ERK)1/2 and Akt-dependent pathways [ 66 ] , which subsequently affects blood-brain barrier permeability and may cause brain impairment by promoting neuroinflammation associated with interleukin-1β and tumor necrosis factor-α [ 67 ] . Aberrant BA signaling in the gut-liver-brain axis may also be an important factor in the pathogenesis of neurodegenerative diseases [ 68 ] .…”

Section: Bioactive Molecules As Mediators Of the Microbiome-gut-liver...mentioning

confidence: 99%

Microbiota-gut-liver-brain axis and hepatic encephalopathy

Lu,

Zhang,

et al. 2024

Microbiome Res Rep

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Hepatic encephalopathy (HE) is a clinical manifestation of neurological and psychiatric abnormalities that are caused by complications of liver dysfunction including hyperammonemia, hyperuricemia, and portal hypertension. Accumulating evidence suggests that HE could be reversed through therapeutic modifications of gut microbiota. Multiple preclinical and clinical studies have indicated that gut microbiome affects the physiological function of the liver, such as the regulation of metabolism, secretion, and immunity, through the gut-liver crosstalk. In addition, gut microbiota also influences the brain through the gut-brain crosstalk, altering its physiological functions including the regulation of the immune, neuroendocrine, and vagal pathways. Thus, key molecules that are involved in the microbiota-gut-liver-brain axis might be able to serve as clinical biomarkers for early diagnosis of HE, and could be effective therapeutic targets for clinical interventions. In this review, we summarize the pathophysiology of HE and further propose approaches modulating the microbiota-gut-liver-brain axis in order to provide a comprehensive understanding of the prevention and potential clinical treatment for HE with a microbiota-targeted therapy.

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The Identification of Key Genes and Biological Pathways in Cardiac Arrest by Integrated Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad,

Vastrad

2024

Preprint

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Cardiac arrest (CA) is a common cause of death world wide. The disease has lacks effective treatment. Efforts have been made to elucidate the molecular pathogenesis of CA, but the molecular mechanisms remain elusive. To identify key genes and pathways in CA, the next generation sequencing (NGS) GSE200117 dataset was downloaded from the Gene Expression Omnibus (GEO) database. DESeq2 tool was used to recognize differentially expressed genes (DEGs). Gene ontology (GO) and REACTOME pathway enrichment analyses were performed to analyze the DEGs and associated signal pathways in the g:Profiler database. The IID database was used to construct the protein-protein interaction (PPI) network, and modules analysis was performed using Cytoscape. A miRNA-hub gene regulatory network and TF-hub gene regulatory network were then constructed to screen miRNAs, TFs and hub genes by miRNet and NetworkAnalyst database and Cityscape software. Receiver operating characteristic curve (ROC) analysis used to verified the hub genes. In total, 844 DEGs were identified, comprising 414 up regulated genes and 430 down regulated genes. GO and REACTOME pathway enrichment analyses indicated that the DEGs for CA were mainly enriched in organonitrogen compound metabolic process, response to stimulus, translation and immune system. Ten hub genes (up-regulated: HSPA8, HOXA1, INCA1 and TP53; down-regulated: HSPB1, LMNA, SNCA, ADAMTSL4 and PDLIM7) were screened. We also predicted miRNAs (hsa-mir-1914-5p and hsa-mir-598-3p) and TFs (JUN and PRRX2) targeting hub genes. This study uses a series of bioinformatics technologies to obtain hug genes, miRNAs and TFs, and key pathways related to CA. These analysis results provide us with new ideas for finding biomarkers and treatment methods for CA.

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Global sphingosine-1-phosphate receptor 2 deficiency attenuates neuroinflammation and ischemic-reperfusion injury after neonatal stroke

Cited by 3 publications

References 53 publications

Immune-Neurovascular Interactions in Experimental Perinatal and Childhood Arterial Ischemic Stroke

Immune-Neurovascular Interactions in Experimental Perinatal and Childhood Arterial Ischemic Stroke

Microbiota-gut-liver-brain axis and hepatic encephalopathy

The Identification of Key Genes and Biological Pathways in Cardiac Arrest by Integrated Bioinformatics and Next Generation Sequencing Data Analysis

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