No Abstract Available.
Gene Expression* ; Neuroglia*

No abstract available.
Calcium* ; Lidocaine* ; Neuroglia* ; Reperfusion*

No abstract available.
Animals ; Mice* ; Neuroglia* ; Theilovirus*

Neuroglia ; Brain ; Biology

Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a subtype of dominantly inherited leukoencephalopathies caused by novel CSF1R gene mutation predominantly affecting the cerebral white matter. High signal lesions on diffusion weighted image (DWI) are characteristic. Herein, we describe a patent with ALSP with a novel mutation. The patient had persistent DWI lesions, worsening white matter changes associated with rapidly progressive clinical symptoms.
Axons ; Diffusion ; Humans ; Leukoencephalopathies ; Neuroglia ; White Matter

NG2-glia are a major type of glial cells that are widely distributed in the central nervous system (CNS). Under physiological conditions, they mainly differentiate into oligodendrocytes and contribute to the myelination of axons, so they are generally called oligodendrocyte progenitor cells. Emerging evidence suggests that NG2-glia not only act as the precursors of oligodendrocytes but also possess many other biological properties and functions. For example, NG2-glia can form synapse with neurons and participate in energy metabolism and immune regulation. Under pathological conditions, NG2-glia can also differentiate into astrocytes, Schwann cells and even neurons, which are involved in CNS injury and repair. Therefore, a deeper understanding of the biological characteristics and functions of NG2-glia under physiological and pathological conditions will be helpful for the treatment of CNS injury and disease. This article reviews the recent advances in the biological characteristics and functions of NG2-glia.
Astrocytes ; Central Nervous System ; Neuroglia ; Neurons ; Oligodendroglia

OBJECTIVE: Growth of cerebral gliomas depends on their neovascularization and invasion into the adjacent neural tissue. There are several extracellular and intracellular factors affecting its growth. Tenascin(TN) is a type of extracellular matrix(ECM) protein which may be responsible for the migration of neoplastic cells and tumor angiogenesis, but its exact role has not been established. We studied the relation between the expression of TN and the histological grade of the glial cell tumors as well as to determine the expression of TN-C in tumor vessel. PATIENTS AND METHODS:In the fifty-six patients with glial cell tumors, we characterized the expression of tenascin-C(TN-C) in the neoplastic vessel, intercellular network, and tumor cell by immunohistochemistry using monoclonal antibody. The relationship between the histological malignancy and TN-C expression was evaluated. In addition, TN-C expression of the tumor vessels was also examined. RESULTS: The tumors included 32 glioblastomas, 13 astrocytomas, 4 pilocytic astrocytoma, 3 anaplastic astrocytoma, 1 pleomorphic xanthoastrocytoma, 1 oligodendroglioma, 1 anaplastic oligodendroglioma, and 1 mixed oligoastrocytoma. TN-C expression in intercellular network of glioblastoma, anaplastic astrocytoma, and astrocytoma was 87. 5%, 66.7%, and 61.5%, respectively. There was a close relationship between the TN-C expression and histological grade of the glial cell tumors. In 28(87.5%) of 32 glioblastomas, TN-C was significantly expressed in the tumor vessels(p<0.05). CONCLUSION: Present results demonstrate that TN-C in the glial cell tumors may be identified as a one of the related factors contributing to malignant progression. And also, enhanced expression of TN-C in the tumor vessels of glioblastoma indicate the possibility that TN-C could be involved in neoplastic angiogenesis.
Astrocytoma ; Glioblastoma ; Glioma* ; Humans ; Immunohistochemistry ; Neuroglia* ; Oligodendroglioma ; Tenascin*

For years, diabetic retinopathy has been defined based on vascular lesions, and neural abnormalities were not regarded as important. This review summarizes evidence that the neural retina has important effects on the retinal vasculature under normal conditions, and the interaction between the retinal neuroglial cells and vascular function is altered in diabetes. Importantly, new evidence raises a possibility that abnormalities within retinal neuroglial cells (notably photoreceptors) might actually be causing or initiating the vascular disease in diabetic retinopathy.
Diabetes Mellitus ; Diabetic Retinopathy ; Neuroglia* ; Retina ; Retinaldehyde* ; Vascular Diseases

Müller glia (MG) are the primary support cells in the vertebrate retina, regulating homeostasis in one of the most metabolically active tissues. In lower vertebrates such as fish, they respond to injury by proliferating and reprogramming to regenerate retinal neurons. In mammals, MG may also react to injury by proliferating, but they fail to initiate regeneration. The barriers to regeneration could be intrinsic to mammalian MG or the function of the niche that cannot support the MG reprogramming required for lineage conversion or both. Understanding these mechanisms in light of those being discovered in fish may lead to the formulation of strategies to unlock the neurogenic potential of MG and restore regeneration in the mammalian retina.
Homeostasis ; Mammals ; Neurogenesis ; Neuroglia* ; Regeneration ; Retina ; Retinal Neurons ; Vertebrates

Hypoxia has been shown to promote inflammation, including the release of proinflammatory cytokines, but it is poorly investigated how hypoxia directly affects inflammasome signaling pathways. To explore whether hypoxic stress modulates inflammasome activity, we examined the effect of cobalt chloride (CoCl2)-induced hypoxia on caspase-1 activation in primary mixed glial cultures of the neonatal mouse brain. Unexpectedly, hypoxia induced by oxygen-glucose deprivation or CoCl2 treatment failed to activate caspase-1 in microglial BV-2 cells and primary mixed glial cultures. Of particular interest, CoCl2-induced hypoxic condition considerably inhibited NLRP3-dependent caspase-1 activation in mixed glial cells, but not in bone marrow-derived macrophages. CoCl2-mediated inhibition of NLRP3 inflammasome activity was also observed in the isolated brain microglial cells, but CoCl2 did not affect poly dA:dT-triggered AIM2 inflammasome activity in mixed glial cells. Our results collectively demonstrate that CoCl2-induced hypoxia may negatively regulate NLRP3 inflammasome signaling in brain glial cells, but its physiological significance remains to be determined.
Animals ; Anoxia ; Brain ; Cobalt ; Cytokines ; Inflammation ; Macrophages ; Mice ; Neuroglia