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Dmd mdx mice have defective oligodendrogenesis, delayed myelin compaction and persistent hypomyelination.

Duchenne muscular dystrophy (DMD) is caused by mutations in the DMD gene, resulting in the loss of dystrophin, a large cytosolic protein that links the cytoskeleton to extracellular matrix receptors in skeletal muscle. Aside from progressive muscle damage, many patients with DMD also have neurological deficits of unknown etiology. To investigate potential mechanisms for DMD neurological deficits, we assessed postnatal oligodendrogenesis and myelination in the Dmdmdx mouse model. In the ventricular-subventricular zone (V-SVZ) stem cell niche, we found that oligodendrocyte progenitor cell (OPC)

Necrostatin-1s Suppresses RIPK1-driven Necroptosis and Inflammation in Periventricular Leukomalacia Neonatal Mice.

Periventricular leukomalacia (PVL), a predominant form of brain injury in preterm survivors, is characterized by hypomyelination and microgl … L. In addition, Nec-1s significantly suppressed hypomyelination and promoted the differentiation of oligodendrocyte precursor cells (OPCs), as demonstrated by the increased expression levels of MBP and Olig2, the decreased expression level of GPR17, a significant increase in the number of CC-1-positive cells, and suppression of myelin ultrastructure impairment. Moreover, the mec …

pH Sensor-Based Engulfment Assays to Measure Phagocytic Activity of Astrocytes.

Astrocytes play a crucial role in eliminating unnecessary synapses, neural debris, and pathogenic proteins such as amyloid β plaque through … ntify the amount of synapses engulfed by multiple glial cells, including astrocytes, microglia, and oligodendrocyte precursor cells, revealing distinct roles and mechanisms of glial phagocytosis in eliminating specific synapse populations from defined neural circuits. These advanced assays provide accurate and efficient means of studying glial phagocytosis, contributing to a bet …

SPI1 инициирует образование нейтрофильных внеклеточных ловушек в множестве склероза через CXCL4.

Множественный склероз (MS) — обычное демиелинирующее заболевание центральной нервной системы, сопровождающееся хроническим воспалением и нейродегенерацией. Нейтрофилы и образование нейтрофильных внеклеточных ловушек (НЕТ) играют важную роль в заболеваниях центральной нервной системы. Spi-1 proto-oncogene (SPI1) является важнейшим регулятором развития и созревания миелиоидных клеток. Однако роль ИЦП1 в РС остается неясной. В рамках этого исследования в мышах была создана модель MS путем введения экспериментального аутоиммунного энцефаломиэлита (EAE). Для изучения воздействия SPI1 после MS было

Совпадение в аннотации оригинала
Multiple sclerosis (MS) is a common demyelinating disease of the central nervous system, accompanied by chronic inflammation and neurodegene … uces the release of proinflammatory cytokines, chemokines, and NETs, and promoted the maturation of oligodendrocyte precursor cells and myelin formation, thereby alleviating MS in mice. Further analysis demonstrated that SPI1 positively regulated CXCL4 transcription. Knockdown of CXCL4 partially reversed the effects of SPI1 overexpression on PMA-induced neutrophils. These result …

Microbial modulation of CNS remyelination in multiple sclerosis: the missing link in gut-brain axis research.

Multiple sclerosis (MS) is a chronic, immune-mediated disorder of the central nervous system (CNS) marked by demyelination and neurodegeneration. While much attention has focused on immune dysregulation and neuroinflammation, the failure of effective remyelination is a key driver of disease progression, especially in progressive MS. Recently, the gut microbiome has emerged as a potent modulator of systemic immunity and CNS function, influencing processes such as neuroinflammation and neurogenesis. This review examines current evidence on microbiota-derived metabolites, including short-chain fa

Возраст и стадия созревания связаны с последствиями фибриногена для человека Олигодендроголии.

Фибриноген — это протеин, полученный из крови и содержащийся в коагуляции, и он может проникнуть в центральную нервную систему (КНС) после разрушения мозгового барьера. Эта молекула была связана с множественным склерозом (MS), заболеванием, отмеченным воспалением и обезвоживанием в CNS. Однако воздействие этой молекулы не изучалось на миелионирующих клетках человека. В этом исследовании рассматривается вопрос о том, как фибриноген влияет на родственные клетки человека олигодендроцита (OL) на различных этапах развития. Используя индуцированные плюрипотентные стволовые клетки (iPSC) прекурсоры O

Adult Neurogenesis of Teleost Fish Determines High Neuronal Plasticity and Regeneration.

Studying the properties of neural stem progenitor cells (NSPCs) in a fish model will provide new information about the organization of neurogenic niches containing embryonic and adult neural stem cells, reflecting their development, origin cell lines and proliferative dynamics. Currently, the molecular signatures of these populations in homeostasis and repair in the vertebrate forebrain are being intensively studied. Outside the telencephalon, the regenerative plasticity of NSPCs and their biological significance have not yet been practically studied. The impressive capacity of juvenile salmon

TNFR1-JNK signaling is the shared pathway of neuroinflammation and neurovascular damage after LPS-sensitized hypoxic-ischemic injury in the immature brain.

BACKGROUND: Hypoxic-ischemia (HI) and inflammation are the two major pathogenic mechanisms of brain injury in very preterm infants. The neurovascular unit is the major target of HI injury in the immature brain. Systemic inflammation may worsen HI by up-regulating neuroinflammation and disrupting the blood-brain barrier (BBB). Since neurons and oligodendrocytes, microvascular endothelial cells, and microglia may closely interact with each other, there may be a common signaling pathway leading to neuroinflammation and neurovascular damage after injury in the immature brain. TNF-α is a key pro-in

MRI Visualization of Melatonin-Promoted Oligodendrogenesis and Its Neuroprotective Effects in Preterm White Matter Injury Rat Model.

Preterm white matter injury (PWMI) is a serious neurologic condition that threatens neonatal survival and severely impairs the cognitive and … al magnetic resonance imaging (MRI) with histological analyses to investigate the effects of Mel on oligodendrocyte precursor cells (OPCs) proliferation, differentiation, and subsequent white matter development. We discovered that Mel administration increased cerebral oxygenation and blood flow, thereby altering the cerebral metabolic microenvironment and mitigating white matter …

Grape Seed Proanthocyanidin Extract (GSPE) Mitigates Preterm White Matter Injury in Mice Via Improving Mitochondrial Homeostasis and Activity of IMMP2L-Related Signaling Pathway.

Grape seed proanthocyanidins extract (GSPE) has demonstrated significant neuroprotective efficacy in various neurodevelopmental disorders, n … yelin damage was evaluated. Mitochondrial homeostasis‌ was detected in PWMI model mice and cultured oligodendrocyte precursor cells (OPCs). Brain tissues from mice groups underwent RNA-seq. A dual-luciferase reporter assay was employed to validate the direct binding interaction between miR-153 and IMMP2L mRNA. The results showed that treatment of GSPE ameliorated cerebral ischem …

miR-124 regulates early isolation-induced social abnormalities via inhibiting myelinogenesis in the medial prefrontal cortex.

Patients with autism spectrum disorder (ASD) typically experience substantial social isolation, which may cause secondary adverse effects on … 24 sponge in the bilateral mPFC, ubiquitously or specifically in oligodendroglia. In cultured mouse oligodendrocyte precursor cells, introducing a synthetic mmu-miR-124 inhibited the differentiation process through suppressing expression of nuclear receptor subfamily 4 group A member 1 (Nr4a1). Overexpressing Nr4a1 in the bilateral mPFC also corrected the social behavioral defic …

An augmentation in histone dimethylation at lysine nine residues elicits vision impairment following traumatic brain injury.

Traumatic Brain Injury (TBI) affects more than 1.7 million Americans each year and about 30% of TBI-patients having visual impairments. The … Nrf2) via direct interaction. The induction of oxidative stress is associated with death in RGC and oligodendrocyte precursor cells (OPCs). The death in OPCs is correlated with a reduction in myelination, and the expression of myelin binding protein (MBP) in association with degeneration of neurofilaments in the optic nerve. This event allied to an impairment of the retrograde t …

Phenotypic shift of astrocytes from A1 to A2 induced by fasudil improves demyelination recovery in cuprizone-treated mice.

Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS), characterized by neuroinflammation, demyelination, and subsequent axonal degeneration. Astrocytes (ASTs) play a dual role in MS pathogenesis, adopting either neurotoxic A1 or neuroprotective A2 phenotypes, which respectively inhibit or promote myelin repair. Fasudil (FSD), a Rho kinase inhibitor, has demonstrated potential in modulating AST phenotypes and facilitating remyelination. In this study, we investigated whether FSD treatment transformed astrocytes from A1 to A2 phenotype in cuprizone-induced

Natural flavonoids in multiple sclerosis: molecular insights and emerging therapeutic strategies.

Multiple sclerosis is a chronic immune mediated disease in which current disease modifying therapies reduce inflammatory relapses but incompletely address neurodegeneration and remyelination. Natural flavonoids are pleiotropic polyphenols that can modulate immune and glial signaling, oxidative stress, and mitochondrial function. This review synthesizes evidence from experimental models and human studies on flavonoids relevant to multiple sclerosis, emphasizing mechanisms involving NF-κB, Nrf2, inflammasome signaling, and microglia and macrophage polarization that shape oligodendrocyte precurso

Distinct microglial and macrophage distribution patterns in the concentric and lamellar lesions in Baló's disease and neuromyelitis optica spectrum disorders.

TMEM119 and purinergic receptor P2Y12 (P2RY12), which are not expressed by recruited peripheral blood macrophages, are proposed to discriminate microglia from macrophages. Therefore, we investigated the distribution patterns of microglia and macrophages in 10 concentric lesions from four autopsied Baló's disease cases and one neuromyelitis optica spectrum disorder (NMOSD) case, using quantitative immunohistochemistry for the markers TMEM119, P2RY12, CD68, CD163 and GLUT5. Three cases with Baló's disease had distal oligodendrogliopathy (DO) showing preferential loss of myelin-associated glycopr

Sustained MicroRNA delivery enhanced remyelination and functional recovery after spinal cord injury.

Myelination by oligodendrocytes (OLs) is critical for central nervous system (CNS) function. It facilitates rapid electrical conduction and supports neuronal metabolism. Unfortunately, spinal cord injury (SCI) disrupts this process by causing OL loss and axonal demyelination. Consequently, profound functional deficits are frequently observed. Although myelination is important, the role of remyelination remains a topic of debate. Numerous studies strongly support the role of remyelination in restoring function after chemically induced demyelination. However, reducing OL-mediated remyelination d

Deletion of PDK1 in oligodendrocyte lineage cells causes white matter abnormality and myelination defect in the central nervous system.

PDK1 (3-Phosphoinositide dependent protein kinase-1) is a member in the PI3K (phosphatidylinositol 3 kinase) pathway and is implicated in neurodevelopmental disease with microcephaly. Although the role of PDK1 in neurogenesis has been broadly studied, it remains unknown how PDK1 may regulate oligogenesis in the central nervous system (CNS). To address this question, we generated oligodendrocyte (OL) lineage cells specific PDK1 conditional knockout (cKO) mice. We find that PDK1 cKOs display abnormal white matter (WM), massive loss of mature OLs and severe defect in myelination in the CNS. In co

N-Acetylglucosamine Selectively Attenuates Neuroinflammation in a Mouse Model of Mitochondrial Dysfunction.

AimMitochondrial dysfunction plays a central role in multiple neurodegenerative diseases, yet the temporal sequence of cellular events under … ared at later disease stages. Early myelin abnormalities were accompanied by an initial increase in oligodendrocyte precursor cells, suggesting a compensatory response to early myelin stress. Oral N-acetylglucosamine supplementation reduced glial activation and neuroinflammatory markers, likely through modulation of inflammatory signaling pathways. Although treatment did not ful …

NgR1 knockout increased neuronal excitability and altered seizure pattern in traumatic brain injury mice brain after PTZ-induced seizure.

The recovery process from traumatic brain injury (TBI) is significantly impeded by inhibitors such as Nogo-A, myelin associated glycoprotein, and oligodendrocyte myelin glycoprotein, which exert an impact on the regeneration and repair of neuronal axons through their binding to Nogo-66 receptor 1 (NgR1). Recent research findings have revealed that NgR1 signaling may play a pivotal role in various seizure mechanisms, including the regulation of synaptic plasticity and migration of neural precursor cells. In this study, wild type (WT) and NgR1 knockout (KO) mice were utilized to establish cranio

NG2-glia cell proliferation and differentiation by glial growth factor 2 (GGF2), a strategy to promote functional recovery after ischemic stroke.

Stroke is the leading cause of adult disability. Spontaneous functional recovery occurs after ischemic stroke, but it is very limited. Therefore, it is urgent to find a strategy to promote functional recovery after stroke in clinical setting. Gray matter damage has received extensive attention owing to the important roles of the gray matter in synaptic plasticity, cognitive, and motor function. However, stroke also causes white matter damage, which accounts for half of the infarct volume and can be aggravated by blood brain barrier damage. Disruption of white matter integrity, which is charact