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[Abstract] Oligodendroglial lineage cells (OLGs) are important cell reserves for myelination and remyelination. Recent studies of central nervous system (CNS) indicated that besides traditional CNS immune cells like microglia, primitive cells of oligodendroglial lineage, oligodendrocyte progenitor cells (OPCs) can also actively participate immune responses. Simulated by physiological or pathological factors, OPCs can express a series of receptors,signaling and/ or regulatory molecules et al, in this way,OPCs can play a critical role in both development and maintenance of the blood-cerebrospinal fluid barrier (BCB), and most essentially, in initial stage for recruitment of peripheral immune cells and initial immune activation. Besides, in neurological disorders, recent research has revealed that OPCs can transform to disease-specific cell states, characterized by activation of immune cell exclusive genes. These findings may provide the basis for a new insight into the therapeutic strategy of neuron disorders and neurovascular diseases by effectively regulating OPCs.
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Oligodendrocyte progenitor cells are distributed throughout the central nervous system and can proliferate, migrate and differentiate into oligodendrocytes. The core function of oligodendrocytes is to produce myelin, form a myelin sheath, wrap the axons, and increase the conduction rate of neurons. Recent studies have shown that large numbers of oligodendrocyte progenitor cells exist in the lesions of neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease, and these cells play an important role in the repair of neurological damage. The physiological functions of oligodendrocyte progenitor cells and their roles in neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease are reviewed in order to provide a new idea and direction for the research and treatment of neurodegenerative diseases.
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Autoimmune epilepsy (AE) is a type of epilepsy mediated by autoantibodies and immune cells. The main pathogenesis of AE is that autoimmune antibodies related to AE interact with surface of nervous cell membrane antigens or intracellular antigens, which leads to the disorder of excitatory and inhibitory nervous system and causes epileptic seizures. Glutamate receptor subunit 3 peptide B antibodies (GluR3B Ab's) are one type of anti-neuron autoantibodies related to AE, and they can combine with GluR3B subunit of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR), which causes an increase of intracellular calcium. Intracellular calcium overload further leads to dysregulation of energy metabolism in neurons or oligodendrocyte progenitor cells (OPCs). The damage of neurons or OPCs eventually trigger seizure. Here, we mainly discuss the mechanisms of GluR3B Ab's involving in the development of autoimmune epilepsy.
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Objective To investigate the protective effect of melatonin and its possible mechanism for repairing in the immature white matter damage due to brain hypoxia-ischemia (HI).Methods Forty-eight three-day SD rats after birth were randomly divided into 3 groups:sham-operated(SHAM) group,HI group and melatonin treatment(MT) group.Periventricular white matter damage (PWMD) to animal models were estabished according to Rice modeling.MT group was treated with melatonin pre-operatively,immediately postoperation,1 hour postoperation and 24 hours postoperation via intraperitoneal injection,and the other groups were injected with the same volume of dissolvent.The rats were executed by decollation after 2 days and 14 days.The histological changes in periventricular white matter were observed by HE staining and immunohistochemistry.Results For the 3 groups,the structure in ope-ration side of the white matter in the peripheral ventricles of the brain 2 days postoperation were significant different (P ＜0.05).The O4 positive cells decreased one by one/greatest in the SHAM group[(75.548 ± 7.333)/hpf] followed by MT group [(59.971 ± 3.635)/hpf],and HI group [(40.511 ± 2.848)/hpf] (P ＜ 0.05).The expression of Casepase-3 increased in the SHAM group (107.724 ± 10.266),MT group (132.289 ± 8.537),and HI group (202.168 ± 14.367),and the difference was statically significant (P ＜ 0.05).Ventricular index was greater in operation side of the white matter in the peripheral ventricles of the 14-day-brain in the SHAM group(0.928 ±0.063),MT group (1.813 ± 0.110),HI group (2.752 ± 0.201),increasingly,while absorbance value of myelin basic protein decreased one by one in sequence(39.504 ± 1.673,21.729 ± 1.614,11.344 ± 1.118).Conclusions MT plays a role in protecting the periventricular white matter via inhibiting the apoptosis of oligodendrocyte progenitor cell,and thus benefits the PWMD.