نتایج جستجو برای: Oligodendrocyte progenitors

تعداد نتایج: 24203  

Journal: :Journal of neuroscience research 1997
J M Redwine K L Blinder R C Armstrong

Basic fibroblast growth factor (bFGF) induces proliferation and alters differentiation of cultured oligodendrocyte lineage cells. In situ, bFGF is present in normal adult central nervous system (CNS) and upregulated during an early stage of various pathological conditions. We examined the expression of receptors for bFGF (FGFRs) by oligodendrocyte progenitors and oligodendrocytes in situ in nor...

Journal: :Neuron 2007
Ye He Jeff Dupree Ju Wang Juan Sandoval Jiadong Li Huifei Liu Yang Shi Klaus Armin Nave Patrizia Casaccia-Bonnefil

The progression of progenitors to oligodendrocytes requires proliferative arrest and the activation of a transcriptional program of differentiation. While regulation of cell cycle exit has been extensively characterized, the molecular mechanisms responsible for the initiation of differentiation remain ill-defined. Here, we identify the transcription factor Yin Yang 1 (YY1) as a critical regulat...

Journal: :Development 2001
Y Qi J Cai Y Wu R Wu J Lee H Fu M Rao L Sussel J Rubenstein M Qiu

Oligodendrocytes are derived from glial precursors that arise from the ventral neural tube early in development. In the developing chicken CNS, oligodendrocyte progenitors selectively express Nkx2.2 homeodomain transcription factor, raising the possibility that Nkx2.2 may directly regulate oligogliogenesis. In this study, we have examined Nkx2.2 expression in rodent glial precursors and studied...

Multiple sclerosis (MS) is an autoimmune disease which affects myelin in the central nervous system (CNS) and leads to serious disability. Currently available treatments for MS mainly suppress the immune system. Regenerative medicine-based approaches attempt to increase myelin repair by targeting endogenous progenitors or transplanting stem cells or their derivatives. Fingolimod exerts anti-inf...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2003
Ju Young Kim Qin Sun Michael Oglesbee Sung Ok Yoon

The knock-out analyses of neuregulin and its receptors have indicated that they play essential roles in Schwann cell development. However, the role they play in oligodendrocyte development in vivo has remained unclear, because such knock-out animals die before CNS myelination begins. We examined the role of neuregulin signaling in the CNS by generating transgenic mice that express a dominant-ne...

2015
Fernando C. Ortiz Maddalena Balia David Orduz

Therapeutic repair of myelin disorders may be limited by the relatively slow rate of human oligodendrocyte differentiation. To identify appropriate pharmacological targets with which to accelerate differentiation of human oligodendrocyte progenitors (hOPCs) directly, we used CD140a/O4-based FACS of human forebrain and microarray to hOPC-specific receptors. Among these, we identified CHRM3, a M3...

Multiple sclerosis (MS) is an autoimmune disease which affects myelin in the central nervous system (CNS) and leads to serious disability. Currently available treatments for MS mainly suppress the immune system. Regenerative medicine-based approaches attempt to increase myelin repair by targeting endogenous progenitors or transplanting stem cells or their derivatives. Fingolimod exerts anti-inf...

2011
Alireza Pouya Leila Satarian Sahar Kiani Mohammad Javan Hossein Baharvand

BACKGROUND This study aims to differentiate human induced pluripotent stem cells (hiPSCs) into oligodendrocyte precursors and assess their recovery potential in a demyelinated optic chiasm model in rats. METHODOLOGY/PRINCIPAL FINDINGS We generated a cell population of oligodendrocyte progenitors from hiPSCs by using embryoid body formation in a defined medium supplemented with a combination o...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2009
Jenne Relucio Iva D Tzvetanova Wei Ao Sabine Lindquist Holly Colognato

Mutations in LAMA2, the gene for the extracellular matrix protein laminin-alpha2, cause a severe muscular dystrophy termed congenital muscular dystrophy type-1A (MDC1A). MDC1A patients have accompanying CNS neural dysplasias and white matter abnormalities for which the underlying mechanisms remain unknown. Here, we report that in laminin-deficient mice, oligodendrocyte development was delayed s...

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