Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation

Back, Stephen A.; Tuohy, Thérèse M.F.; Chen, Hanqin; Wallingford, Nicholas; Craig, Andrew; Struve, Jaime; Luo, Ning; Banine, Fatima; Liu, Ying; Chang, Ansi; Trapp, Bruce D.; Bebo, Bruce F.; Rao, Mahendra S.; Sherman, Larry S.

doi:10.1038/nm1279

Cited by 534 publications

(533 citation statements)

References 44 publications

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“…The glycosaminoglycan hyaluronan is another component found to inhibit OPC differentiation and remyelination [45]. Hyaluronan has been observed to accumulate in chronic MS lesions and in mice with experimental autoimmune encephalomyelitis (EAE).…”

Section: Hyaluronanmentioning

confidence: 99%

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

et al. 2011

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Regeneration of myelin sheaths (remyelination) after central nervous system demyelination is important to restore saltatory conduction and to prevent axonal loss. In multiple sclerosis, the insufficiency of remyelination leads to the irreversible degeneration of axons and correlated clinical decline. Therefore, a regenerative strategy to encourage remyelination may protect axons and improve symptoms in multiple sclerosis. We highlight recent studies on factors that influence endogenous remyelination and potential promising pharmacological targets that may be considered for enhancing central nervous system remyelination.

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Section: Hyaluronanmentioning

confidence: 99%

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

et al. 2011

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“…It can bind hyaluronan, ERK kinase and microtubules and participates in cell motility, signaling, and oncogenic events (Maxwell et al 2005). It has been reported that hyaluronan, one of the ligands of HAMMR, accumulates in demyelinated lesions and inhibits OPC maturation through binding to CD44, another receptor of hyaluronan (Back et al 2005). The high expression of HAMMR on OPCs implicated that HAMMR might be another CD44-like receptor which can mediate hyaluronan to maintain self-renewal of OPCs.…”

Section: Gene Profiles Of Opcsmentioning

confidence: 99%

Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes

Wang

Zhou

et al. 2011

Tohoku J. Exp. Med.

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Oligodendrocyte precursor cells (OPCs) are bipotential progenitor cells that can differentiate into myelin-forming oligodendrocytes or functionally undetermined type II astrocytes. Transplantation of OPCs is an attractive therapy for demyelinating diseases. However, due to their bipotential differentiation potential, the majority of OPCs differentiate into astrocytes at transplanted sites. It is therefore important to understand the molecular mechanisms that regulate the transition from OPCs to oligodendrocytes or astrocytes. In this study, we isolated OPCs from the spinal cords of rat embryos (16 days old) and induced them to differentiate into oligodendrocytes or type II astrocytes in the absence or presence of 10% fetal bovine serum, respectively. RNAs were extracted from each cell population and hybridized to GeneChip with 28,700 rat genes. Using the criterion of fold change > 4 in the expression level, we identified 83 genes that were up-regulated and 89 genes that were down-regulated in oligodendrocytes, and 92 genes that were up-regulated and 86 that were down-regulated in type II astrocytes compared with OPCs. The up-regulated genes, such as activating transcription factor 3 and myelin basic protein in oligodendrocytes or claudin 11 in type II astrocytes, might contribute to OPC differentiation and represent constitutive components of oligodendrocytes or type II astrocytes. The down-regulated genes in both oligodendrocytes and type II astrocytes, such as transcription factor 19, might be involved in maintaining self-renewal and/or represent the property of OPCs. These results provide new insights into the elucidation of the molecular mechanisms, by which OPCs differentiate to oligodendrocytes or type II astrocytes.

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“…These hydrogel systems express mechanical properties similar to that of brain tissue and can be altered through photo cross-linking systems, testing a variety of compressive moduli. In normal tissue, hyaluronan has a range of molecular weights that play critical rolls in controlling cell motility, cell growth, and angiogenesis (Back et al, 2005). Engrafting transplanted mouse, human progenitor, and human glial-restricted precursor cells in HA-PEG gels demonstrates prolonged survival in the xenograft, despite the induction of a mild inflammatory response after 2 weeks (Liang et al, 2013).…”

Section: Hyaluronic Acid (Ha)mentioning

confidence: 99%

Stroke Repair via Biomimicry of the Subventricular Zone

Matta

Gonzalez

2018

Front. Mater.

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Stroke is among the leading causes of death and disability worldwide, 85% of which are ischemic. Current stroke therapies are limited by a narrow effective therapeutic time and fail to effectively complete the recovery of the damaged area. Magnetic resonance imaging of the subventricular zone (SVZ) following infarct/stroke has allowed visualization of new axonal connections and projections being formed, while new immature neurons migrate from the SVZ to the peri-infarct area. Such studies suggest that the SVZ is a primary source of regenerative cells for the repair and regeneration of stroke-damaged neurons and tissue. Therefore, the development of tissue engineered scaffolds that serve as a bioreplicative SVZ niche would support the survival of multiple cell types that reside in the SVZ. Essential to replication of the human SVZ microenvironment is the establishment of microvasculature that regulates both the healthy and stroke-injured blood-brain barrier, which is dysregulated poststroke. In order to reproduce this niche, understanding how cells interact in this environment is critical, in particular neural stem cells, endothelial cells, pericytes, ependymal cells, and microglia. Remodeling and repair of the matrix-rich SVZ niche by endogenous reparative mechanisms may then support functional recovery when enhanced by an artificial niche that supports the survival and proliferation of migrating vascular and neuronal cells. Critical considerations to mimic this area include an understanding of resident cell types, delivery method, and the use of biocompatible materials. Controlling stem cell survival, differentiation, and migration are key factors to consider when transplanting stem cells. Here, we discuss the role of the SVZ architecture and resident cells in the promotion and enhancement of endogenous repair mechanisms. We elucidate the interplay between the extracellular matrix composition and cell interactions prior to and following stroke. Finally, we review current cell and neuronal niche biomimetic materials that allow for a tissue-engineered approach in order to promote structural and functional restoration of neural circuitry. By creating an artificial mimetic SVZ, tissue engineers can strive to facilitate tissue regeneration and functional recovery.

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Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation

Cited by 534 publications

References 44 publications

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

Myelin Regeneration in Multiple Sclerosis: Targeting Endogenous Stem Cells

Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes

Stroke Repair via Biomimicry of the Subventricular Zone

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