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Methylprednisolone Promote the Migration of Oligodendrocyte Precursor Cells

Author: ShenWeiRan
Tutor: HeCheng
School: Second Military Medical University
Course: Neurobiology
Keywords: Oligodendrocytes precursor cells Migrate Methylprednisolone Glucocorticoid receptor ERK
CLC: R744
Type: Master's thesis
Year: 2010
Downloads: 16
Quote: 0
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Abstract

Jumping nerve impulse conduction depends on the formation of the myelin sheath. Myelin structure is projecting by the differentiation and maturation oligonucleotide specialized glial cells lamellar structure dense enveloping axons formed. For axon protection, nutrition, and other functions. The myelin sheath of the nervous system normal exercise the functions necessary ingredients. Oligodendrocytes from development by oligodendrocytes precursor cells (oligodendrocyte precursor cells, OPC). OPC in developmental proliferation, migration, differentiation and development stage, finally wrapping axons and myelin formation. OPC originated in a very limited area of ??the nervous system. First group of OPC originates in the brain in the subventricular zone (subventricular zone, SVZ), and the precursor region originated in the motor neurons in the spinal cord. After long-distance migration in a very short time, and spread to the entire development process of the central nervous system (central nervous system, CNS). Whether in the body or outside the culture conditions, OPC has a strong athletic ability. Has identified a variety of impacts OPC migration factor, but the the OPC migration path and molecular mechanisms there are a lot of unknowns at. Human beings, there are a lot of diseases associated with myelin. Including spinal cord injury (spinal cord injury, SCI), demyelinating disease (demyelination disease), Alzheimer's disease. The common characteristic of these diseases is myelin loss. Treatment of such diseases not only to reduce the damage continues, and to repair existing damage. The study found that the existence of the phenomenon of spontaneous myelin repair the patient's body, and that remyelination process. The predecessors has confirmed, there are still a certain percentage of the adult central nervous system the OPC, pathological injury OPC will be activated to the injury site, and continue to migrate from the SVZ accurate. The remyelination process equivalent to reproduce the various stages of the OPC development process, namely migration, differentiation, and into myelin. The migration process is OPC repair damaged myelin first need to complete the steps. Undoubtedly help to promote OPC migration accelerated remyelination process. Therefore, both from the point of view or physiological development of the migration process is of great significance from the perspective of pathological studies of OPC. Methylprednisolone (methylprednisolone, Mep) is a commonly used drug for the clinical treatment of spinal cord injury and multiple sclerosis (multiple sclerosis, MS). Mep is a synthetic glucocorticoid analogues, which inhibit the activation of the immune system and inflammatory responses as an immune system quenched, thereby reducing the loss of the immune system attacks on the nervous system and myelin. Symptoms have been alleviated to give Mep merely the Mep immunosuppressive effects, Mep For OPC itself what role, especially for OPC migration would affect is very meaningful. The subject of the study confirmed the Mep promote OPC cell migration and activation of ERK1 / 2 phosphorylation dependent glucocorticoid receptor (glucocorticoid receptor, GR). The main results of this study are as follows: 1. Vitro purified and cultured OPC. Cultured cells purified cells, consistent with the literature, the typical OPC was bipolar expression of OPC molecular markers NG2, A285, and can differentiate into the different stages of O4-positive, O1-positive or MBP positive oligodendrocytes lineage cells. OPC migration 2.Mep promote. Use of Transwell detection 100nM, 1μM Mep OPC migration has a significant role in promoting. Matri gel mobility shift assay model confirmed that, a 1μM concentration Mep-treated cells after the ball, move out of the number of cells increased significantly. 3.Mep has no effect on the proliferation of the OPC. BrdU incorporation experiments show, incorporation BrdU4 hours OPC BrdU-positive rate of about 30%, do not join with the Mep change. 4.OPC expression of the glucocorticoid receptor. Glucocorticoid receptor expression can be detected by RT-PCR, Western-blot and immune cells staining. The role of the 5.Mep promote OPC migration glucocorticoid receptor-dependent. The Transwell migration models the GR antagonist Ru38486 in can block Mep promote migration role of OPC. GR endogenous ligand corticosterone, promote OPC migration Mep same role. 6.Mep promote OPC migration is mediated by ERK pathway. Western blot, Mep sustained activation of ERK1 / 2 up to 4 hours. Transwell model of ERK1 / 2 blocker PD98059 can block Mep promote migration role of OPC JNK inhibitor SP600125.

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