AI Article Synopsis
Article Abstract
White matter (WM) is a highly prominent feature in the human cerebrum and is comprised of bundles of myelinated axons that form the connectome of the brain. Myelin is formed by oligodendrocytes and is essential for rapid neuronal electrical communication that underlies the massive computing power of the human brain. Oligodendrocytes are generated throughout life by oligodendrocyte precursor cells (OPCs), which are identified by expression of the chondroitin sulphate proteoglycan NG2 (Cspg4), and are often termed NG2-glia. Adult NG2+ OPCs are slowly proliferating cells that have the stem cell-like property of self-renewal and differentiation into a pool of 'late OPCs' or 'differentiation committed' OPCs(COPs) identified by specific expression of the G-protein-coupled receptor GPR17, which are capable of differentiation into myelinating oligodendrocytes. In the adult brain, these reservoirs of OPCs and COPs ensure rapid myelination of new neuronal connections formed in response to neuronal signalling, which underpins learning and cognitive function. However, there is an age-related decline in myelination that is associated with a loss of neuronal function and cognitive decline. The underlying causes of myelin loss in ageing are manifold, but a key factor is the decay in OPC 'stemness' and a decline in their replenishment of COPs, which results in the ultimate failure of myelin regeneration. These changes in ageing OPCs are underpinned by dysregulation of neuronal signalling and OPC metabolic function. Here, we highlight the role of purine signalling in regulating OPC self-renewal and the potential importance of GPR17 and the P2X7 receptor subtype in age-related changes in OPC metabolism. Moreover, age is the main factor in the failure of myelination in chronic multiple sclerosis and myelin loss in Alzheimer's disease, hence understanding the importance of purine signalling in OPC regeneration and myelination is critical for developing new strategies for promoting repair in age-dependent neuropathology.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8076121 | PMC |
| http://dx.doi.org/10.1007/s00424-021-02544-z | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The JNK Signaling Pathway Regulates Seizures Through ENT1 in Pilocarpine-Induced Epilepsy Rat Model.
CNS Neurosci Ther
December 2024
The Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, Guizhou, China.
Objective: The study investigates whether the expression and function of ENT1 can be regulated by inhibiting the JNK signaling pathway, thereby altering the levels of extracellular adenosine and glutamate in neurons, and subsequently affecting the progression of epilepsy.
Methods: The adult male SD rats were randomly divided into four groups: EP + SP600125 group, EP + DMSO group, EP group, and normal control group. The expression levels of ENT1, p-JNK, and JNK in the hippocampus of rats from each experimental group were detected using Western blotting technology.
The cytokinin efflux transporter ABCC4 participates in Arabidopsis root system development.
Plant Physiol
December 2024
Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan.
The directional and sequential flow of cytokinin in plants is organized by a complex network of transporters. Genes involved in several aspects of cytokinin transport have been characterized; however, much of the elaborate system remains elusive. In this study, we used a transient expression system in tobacco (Nicotiana benthamiana) leaves to screen Arabidopsis (Arabidopsis thaliana) transporter genes and isolated ATP-BINDING CASSETTE TRANSPORTER C4 (ABCC4).
View Article and Find Full Text PDFStudy on the Mechanism of UMI-77 in the Treatment of Sepsis-Induced Acute Lung Injury Based on Transcriptomics and Metabolomics.
J Inflamm Res
December 2024
Department of Critical Care Medicine, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, 317000, People's Republic of China.
Introduction: Sepsis-induced acute lung injury (ALI), a critical sequela of systemic inflammation, often progresses to acute respiratory distress syndrome, conferring high mortality. Although UMI-77 has demonstrated efficacy in mitigating lung injury in sepsis, the molecular mechanisms underlying its action have not yet been fully elucidated.
Methods: This study aimed to delineate the mechanism by which UMI-77 counteracts sepsis-induced ALI using comprehensive transcriptomic and metabolomic analyses.
Network-based meta-analysis and confirmation of genes ATP1A2, FXYD1, and ADCY3 associated with cAMP signaling in breast tumors compared to corresponding normal marginal tissues.
Cell Mol Biol (Noisy-le-grand)
November 2024
Department of Photo Healing and Regeneration, Medical Laser Research Center, Yara Institute, Academic Center for Education, Culture, and Research(ACECR), Tehran, Iran.
Breast cancer (BC) is a global health concern with a growing prevalence. Since BC is a heterogeneous cancer, transcriptome analyzes were carried out on breast tumor tissues relative to their corresponding normal tissues in order to identify gene expression signatures and perform meta-analysis. Five expression profiling by array data sets from breast tumor tissues and non-tumor neighboring tissues were retrieved following a search in the GEO database (GSE70947, GSE70905, GSE10780, GSE29044, and GSE42568).
View Article and Find Full Text PDFMETTL3, m6A modification, and EGR1: interplay affecting myocardial I/R injury outcomes.
Cell Biol Toxicol
December 2024
Department of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.
The occurrence of severe myocardial ischemia/reperfusion (I/R) injury is associated with the clinical application of reestablishment technique for heart disease, and understanding its underlying mechanisms is currently an urgent issue. Prior investigations have demonstrated the potential enhancement of MIRI through EGR1 suppression, although the precise underlying regulatory pathways require further elucidation. The core focus of this investigation is to examine the molecular pathways through EGR1 regulates mitophagy-mediated myocardial cell pyroptosis and its impact on MIRI.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!