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Protective effects of N-acetyl-L-cysteine in human oligodendrocyte progenitor cells and restoration of motor function in neonatal rats with hypoxic-ischemic encephalopathy.

Objective. Since oligodendrocyte progenitor cells (OPCs) are the target cells of neonatal hypoxic-ischemic encephalopathy (HIE), the present study was aimed at investigating the protective effects of N-acetyl-l-cysteine (NAC), a well-known antioxidant and precursor of glutathione, in OPCs as well as in neonatal rats. Methods. In in vitro study, protective effects of NAC on KCN cytotoxicity in F3.Olig2 OPCs were investigated via MTT assay and apoptotic signal analysis. In in vivo study, NAC was administered to rats with HIE induced by hypoxia-ischemia surgery at postnatal day 7, and their motor

Layer I neocortical ectopia: cellular organization and local cortical circuitry.

Focal cortical dysplasia (FCD) are associated with neurological disorders and cognitive impairments in humans. Molecular layer ectopia, clus … nin (CR). Ectopia also contains astrocytes, positive for glial fibrillary acidic protein (GFAP) and oligodendrocyte precursor cells positive for NG2 proteoglycan (NG2). Lastly, we provide electrophysiological and morphological evidence to demonstrate that cells within ectopia receive input from cells within layers I, upper and deeper II/III, and V and provide outputs to cells wi …

The role of induced pluripotent stem cell (IPs) in the transplantation of glaucoma.

AIM: Glaucoma is a heterogeneous group of optic diseases that affect almost 1% to 2% of the population older than 40 years. There are many t … survival was also seen at the 4th week. Immunohistochemical analysis showed that a large number of oligodendrocyte precursor cells (OPCs), positive for the nuclear marker Olig2, survived in the vitreous, proximal to the inner surface of the retina, in glaucomatous eye for up to four weeks. CONCLUSION: Differentiating IPs cells within the glaucomatous eye produced cells that ex …

Single-Cell Transcriptomic Profiling of Brain Cells in Newborn Rats Following Hypoxic Ischemic Encephalopathy.

Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological condition associated with high rates of mortality or long-term disab … or necrosis factors, involvement of microglia in phagocytosis, Stat3-mediated ischemic responses in oligodendrocyte precursor cells, and an increase in senescent lymphatic endothelial cells. In the acute phase, astrocytes were activated and involved in gliogenesis, while microglia proliferated. Neuroblasts were affected by metal ions, and oligodendrocytes decreased. In the subac …

FTY720 (Fingolimod) reverses α-synuclein-induced downregulation of brain-derived neurotrophic factor mRNA in OLN-93 oligodendroglial cells.

Multiple system atrophy (MSA) is a demyelinating neurodegenerative disorder characterized by accumulation of aggregated α-synuclein (aSyn) inside oligodendrocyte precursors, mature oligodendroglia, and neurons. MSA dysfunction is associated with loss of trophic factor production by glial and neuronal cells. Here, we report that recombinant wild type human aSyn uptake by OLN-93, an oligodendroglia cell-line, reduced brain-derived neurotrophic factor (BDNF) expression. Furthermore, OLN-93 cells stably transfected with human wild type or an MSA-associated mutant aSyn, A53E that produces neuronal

Effects Of Ethanol on the Structure and Function of the BBB and Their Roles in Central Nervous System Diseases.

The blood-brain barrier (BBB) plays a vital role in maintaining brain homeostasis, as its proper function and structural integrity are essen … endothelial cells, activates astrocytes and microglia, disrupts the differentiation and survival of oligodendrocyte precursor cells (OPCs), triggers neuroimmune responses, inhibits glucose transport, modifies blood pressure, and increases blood flow. Moreover, we examine how different levels of ethanol consumption influence the risk of developing conditions like Alzheimer's dise …

Метаболический перепрограммирование глиальных клеток: пути жирной кислоты в качестве регулятора ремиэлизации в множестве склероза.

Множественный склероз (MS) — аутоиммунное расстройство, характеризующееся нейроинфламмацией и постепенным демиэлированием, приводящим к необратимым нейронным повреждениям и инвалидности. Несмотря на то, что текущее иммунодуляторное лечение медленно развивается, они не могут эффективно стимулировать регенерацию миелина. В недавних исследованиях подчеркивалась критическая роль глиевых клеток - микроглии, астроцитов и олигодендроцитов - в ремонте миелина, при этом метаболизм жирной кислоты (FA) становится центральным регулятором этого процесса. Жирные кислоты необходимы не только для поддержания

Совпадение в аннотации оригинала
Multiple sclerosis (MS) is an autoimmune disorder characterized by neuroinflammation and progressive demyelination, resulting in irreversibl … ir reactive states can either promote or inhibit myelin repair, depending on the metabolic context. Oligodendrocyte precursor cells, crucial for myelin regeneration, are also regulated by fatty acids, impacting their differentiation and survival. Disruptions in FA metabolism or imbalanced glial activation can impair remyelination, underscoring the need for therapies targeting th …

Spatial transcriptomics reveal heterogeneous cell‒cell interactions among brain regions in cuprizone model consistent with multiple sclerosis lesions.

The cuprizone (CPZ) model is widely used for modeling demyelination in multiple sclerosis (MS) and for testing potential remyelination thera … ihood of interaction between oligodendroglia and microglia, and a novel interaction between MOL and oligodendrocyte precursor cells (OPC), underscoring their roles during de- and remyelination. Finally, astrocytes in the CPZ model had the greatest preservation of disease-associated modules in MS lesions, while MOL, OPC, and microglia showed moderate to low preservation, which ov …

In vivo spatiotemporal dynamics of astrocyte reactivity following neural electrode implantation.

Brain computer interfaces (BCIs), including penetrating microelectrode arrays, enable both recording and stimulation of neural cells. Howeve … evice encapsulation that are spatiotemporally distinct from other glial cells, such as microglia or oligodendrocyte precursor cells. This detailed characterization of astrocyte reactivity will help to better understand the tissue response to intracortical devices and lead to the development of more effective intervention strategies to improve the functional performance of neural …

Selective activation of cannabinoid receptor-2 reduces white matter injury via PERK signaling in a rat model of traumatic brain injury.

BACKGROUND AND PURPOSE: Traumatic brain injury (TBI) destroys white matter, and this destruction is aggravated by secondary neuroinflammator … omic preservation of myelinated axons revealed by DTI and TEM. JWH133 also increased the numbers of oligodendrocyte precursor cells and mature oligodendrocytes. Furthermore, JWH133 drove microglial polarization toward the protective M2 phenotype and modulated the redistribution of microglia in the striatum. Further investigation of the underlying mechanism revealed that JWH133 d …

Repair Mechanisms of the Neurovascular Unit after Ischemic Stroke with a Focus on VEGF.

The functional neural circuits are partially repaired after an ischemic stroke in the central nervous system (CNS). In the CNS, neurovascular units, including neurons, endothelial cells, astrocytes, pericytes, microglia, and oligodendrocytes maintain homeostasis; however, these cellular networks are damaged after an ischemic stroke. The present review discusses the repair potential of stem cells (i.e., mesenchymal stem cells, endothelial precursor cells, and neural stem cells) and gaseous molecules (i.e., nitric oxide and carbon monoxide) with respect to neuroprotection in the acute phase and

Glucose-dependent spatial and temporal modulation of oligodendrocyte progenitor cell proliferation via ACLY-regulated histone acetylation.

How it is determined whether postnatal oligodendrocyte progenitor cells (OPCs) will survive, proliferate or differentiate remains unclear. Here we suggest that temporal and brain regional fluctuations of glucose, concomitant with changes in vascularization, modulate OPC population dynamics. We found that regions with high glucose levels exhibited greater OPC proliferation and histone acetylation than regions with low glucose and that this was mediated by the enzyme ATP-citrate lyase (ACLY), which converts glucose-derived citrate to acetyl-CoA. Mice with Acly deletion in OPCs showed a transient

Platelets regulate neural and oligodendroglial progenitors when infiltrating the brain parenchyma.

The mammalian, including the human, postnatal brain harbors distinct neurogenic and oligodendrogenic progenitor populations, whose activity during homeostasis and degeneration is closely related to blood vessels. Here, we investigated the regulatory role of platelets, that are easily and unlimitedly accessible and can modulate tissue regeneration. In co-cultures, platelets created a pro-stemness environment for neural stem/progenitor cells (NSPCs) and enhanced the differentiation of oligodendrocyte progenitor cells. The effects were dependent on platelet numbers and the culture microenvironmen

Iron deficiency in astrocytes alters cellular status and impacts on oligodendrocyte differentiation.

Iron deficiency (ID) has been shown to affect central nervous system (CNS) development and induce hypomyelination. Previous work from our laboratory in a gestational ID model showed that both oligodendrocyte (OLG) and astrocyte (AST) maturation was impaired. To explore the contribution of AST iron to the myelination process, we generated an in vitro ID model by silencing divalent metal transporter 1 (DMT1) in AST (siDMT1 AST) or treating AST with Fe3+ chelator deferoxamine (DFX; DFX AST). siDMT1 AST showed no changes in proliferation but remained immature. Co-cultures of oligodendrocyte precur

Connexin 43 deletion in astrocytes promotes CNS remyelination by modulating local inflammation.

As the most abundant gap junction protein in the central nervous system (CNS), astrocytic connexin 43 (Cx43) maintains astrocyte network homeostasis, affects oligodendroglial development and participates in CNS pathologies as well as injury progression. However, its role in remyelination is not yet fully understood. To address this issue, we used astrocyte-specific Cx43 conditional knockout (Cx43 cKO) mice generated through the use of a hGFAP-cre promoter, in combination with mice carrying a floxed Cx43 allele that were subjected to lysolecithin so as to induce demyelination. We found no signi

Elevated serum concentrations of HE4 as a novel biomarker of disease severity and renal fibrosis in kidney disease.

OBJECTIVE: The occurrence of epilepsy is associated with myelin sheath injury; oligodendrocyte (OL) is the main cell of myelin sheath; In this study, we observed the changes of OL, demyelination, and myelin associated protein in different stages of intractable epilepsy (IE) at the epileptic foci of patients, and provide useful information for the pathophysiology of IE. PATIENTS AND METHODS: IE patients who received epileptogenic focus resection were recruited as the experimental group, their medical records were collected and postoperative follow-up was performed. The brain tissues from10 cas

Insufficient OPC migration into demyelinated lesions is a cause of poor remyelination in MS and mouse models.

Failure of remyelination of multiple sclerosis (MS) lesions contributes to neurodegeneration that correlates with chronic disability in patients. Currently, there are no available treatments to reduce neurodegeneration, but one therapeutic approach to fill this unmet need is to promote remyelination. As many demyelinated MS lesions contain plentiful oligodendrocyte precursor cells (OPCs), but no mature myelinating oligodendrocytes, research has previously concentrated on promoting OPC maturation. However, some MS lesions contain few OPCs, and therefore, remyelination failure may also be second…

DPSCs-Exos promote OPCs differentiation and white matter repair via Myl9-mediated PRMT5 nucleation after ischemic stroke.

Ischemic stroke often leads to white matter damage due to impaired oligodendrocyte precursor cells (OPCs) differentiation, hindering post-stroke recovery. While dental pulp stem cells-derived exosomes (DPSCs-Exos) have shown promise in stroke recovery, the underlying mechanisms remain unclear. Toward this aim, we investigated the therapeutic potential of DPSCs-Exos for promoting OPCs differentiation and white matter repair after ischemic stroke using in vivo (middle cerebral artery occlusion, MCAO) and in vitro (oxygen-glucose deprivation/reoxygenation, OGD/R) models. Intracerebroventricular D…

Ectopic expression of the immune adaptor protein CD3zeta in neural stem/progenitor cells disrupts cell-fate specification.

Immune signaling and neuroinflammatory mediators have recently emerged as influential variables that regulate neural precursor/stem cell (NPC) behavior and function. In this study, we investigated whether the signaling adaptor protein CD3ζ, a transmembrane protein involved in T cell differentiation and function and recently shown to regulate neuronal development in the central nervous system (CNS), may have a role in NPC differentiation. We analyzed the expression profile of CD3ζ in embryonic rat brain during neurogenic periods and in neurosphere-derived neural cells, and we investigated the a

Therapeutic targeting of differentiation-state dependent metabolic vulnerabilities in diffuse midline glioma.

H3K27M diffuse midline gliomas (DMG), including diffuse intrinsic pontine gliomas (DIPG), exhibit cellular heterogeneity comprising less-differentiated oligodendrocyte precursors (OPC)-like stem cells and more differentiated astrocyte (AC)-like cells. Here, we establish in vitro models that recapitulate DMG-OPC-like and AC-like phenotypes and perform transcriptomics, metabolomics, and bioenergetic profiling to identify metabolic programs in the different cellular states. We then define strategies to target metabolic vulnerabilities within specific tumor populations. We show that AC-like cells