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Oligodendrocyte (OL) damage and death are prominent features of multiple sclerosis (MS) pathology, yet mechanisms contributing to OL loss are incompletely understood. Dysfunctional RNA binding proteins (RBPs), hallmarked by nucleocytoplasmic mislocalization and altered expression, have been shown to result in cell loss in neurologic diseases, including in MS. Since we previously observed that the...
Genomic analyses have revealed heterogeneity among glial progenitor cells (GPCs), but the compartment selectivity of human GPCs (hGPCs) is unclear. Here, we asked if GPCs of human grey and white brain matter are distinct in their architecture and associated gene expression. RNA profiling of NG2‐defined hGPCs derived from adult human neocortex and white matter differed in their expression of genes...
Healthy myelin sheaths consist of multiple compacted membrane layers closely encasing the underlying axon. The ultrastructure of CNS myelin requires specialized structural myelin proteins, including the transmembrane‐tetraspan proteolipid protein (PLP) and the Ig‐CAM myelin‐associated glycoprotein (MAG). To better understand their functional relevance, we asked to what extent the axon/myelin‐units...
Multiple sclerosis (MS) is the most common inflammatory, demyelinating and neurodegenerative disease of the central nervous system in young adults. Chronic‐relapsing experimental autoimmune encephalomyelitis (crEAE) in Biozzi ABH mice is an experimental model of MS. This crEAE model is characterized by an acute phase with severe neurological disability, followed by remission of disease, relapse of...
Inflammation is a common feature in neurodegenerative diseases that contributes to neuronal loss. Previously, we demonstrated that the basal inflammatory tone differed between brain regions and, consequently, the reaction generated to a pro‐inflammatory stimulus was different. In this study, we assessed the innate immune reaction in the midbrain and in the striatum using an experimental model of Parkinson's...
In the central nervous system (CNS), insulin‐like growth factor 1 (IGF‐1) regulates myelination by oligodendrocyte (ODC) precursor cells and shows anti‐apoptotic properties in neuronal cells in different in vitro and in vivo systems. Previous work also suggests that IGF‐1 protects ODCs from cell death and enhances remyelination in models of toxin‐induced and autoimmune demyelination. However, since...
In response to central nervous system (CNS) injury, astrocytes go through a series of alterations, referred to as reactive astrogliosis, ranging from changes in gene expression and cell hypertrophy to permanent astrocyte borders around stromal cell scars in CNS lesions. The mechanisms underlying injury‐induced reactive astrocytes in the adult CNS have been extensively studied. However, little is known...
ADGRG1 (also called GPR56) plays critical roles in brain development and wiring, including cortical lamination, central nervous system (CNS) myelination, and developmental synaptic refinement. However, the underlying mechanism(s) in mediating such diverse functions is not fully understood. Here, we investigate the function of one specific alternative splicing isoform, the GPR56 splice variant 4 (S4),...
A major hallmark of neuroinflammation is the activation of microglia and astrocytes with the induction of inflammatory mediators such as IL‐1β, TNF‐α, iNOS, and IL‐6. Neuroinflammation contributes to disease progression in a plethora of neurological disorders ranging from acute CNS trauma to chronic neurodegenerative disease. Posttranscriptional pathways of mRNA stability and translational efficiency...
NOX4 is a major reactive oxygen species‐producing enzyme that modulates cell stress responses. We here examined the effect of Nox4 deletion on demyelination–remyelination, the most common pathological change in the brain. We used a model of cuprizone (CPZ)‐associated demyelination–remyelination in wild‐type and Nox4‐deficient (Nox4−/−) mice. While the CPZ‐induced demyelination in the corpus callosum...
The unfolded protein response (UPR) is a signal transduction network that responds to endoplasmic reticulum (ER) stress by coordinating protein homeostasis to maintain cell viability. The UPR can also trigger cell death when adaptive responses fail to improve protein homeostasis. Despite accumulating evidence suggesting that the UPR plays a role in neurodegenerative diseases and brain insults, our...
Deficiency of glutamate transporter GLAST in Müller cells may be culpable for excessive extracellular glutamate, which involves in retinal ganglion cell (RGC) damage in glaucoma. We elucidated how GLAST was regulated in rat chronic ocular hypertension (COH) model. Western blot and whole‐cell patch‐clamp recordings showed that GLAST proteins and GLAST‐mediated current densities in Müller cells were...