Genetic fate mapping of Olig2 progenitors in the injured adult cerebral cortex reveals preferential differentiation into astrocytes

Tatsumi, Kouko; Takebayashi, Hirohide; Manabe, Takayuki; Tanaka, Kenji F.; Makinodan, Manabu; Yamauchi, Takahira; Makinodan, Eri; Matsuyoshi, Hiroko; Okuda, Hiromichi; Ikenaka, Kazuhiro; Wanaka, Akio

doi:10.1002/jnr.21862

Cited by 108 publications

(102 citation statements)

References 51 publications

(66 reference statements)

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“…These findings suggest that Olig2 expression can promote the extent of OL specification in the injured adult spinal cord as it does during development. Several recent studies have implicated Olig2 in astrocytic differentiation during development and af- ter injury Tatsumi et al, 2008). However, we were unable to identify any significant difference in the proportion of GFAP positive cells by Olig1 or both Olig1 and Olig2 in combination.…”

Section: Olig1 and Olig2 Cooperatively Regulate The Differentiation Ocontrasting

confidence: 85%

Differential and cooperative actions of Olig1 and Olig2 transcription factors on immature proliferating cells after contusive spinal cord injury

Kim

Hwang

Choi

et al. 2011

Glia

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Section: Olig1 and Olig2 Cooperatively Regulate The Differentiation Ocontrasting

confidence: 85%

Differential and cooperative actions of Olig1 and Olig2 transcription factors on immature proliferating cells after contusive spinal cord injury

Kim

Hwang

Choi

et al. 2011

Glia

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“…2). It is expressed by reactive astrocytes in different injury models [91,92] and its translocation from the nucleus to the cytoplasm in proliferating glial progenitors has been suggested to mediate differentiation into reactive astrocytes [93,94]. Further, genetic…”

Section: Intracellular Transduction Pathways and Cellular Reactivitymentioning

confidence: 99%

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Buffo

Rolando

Ceruti

2010

Biochemical Pharmacology

287

260

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 Running title: Beneficial and detrimental outcomes of astrogliosis after central nervous system injury. Abbreviations:Ado, adenosine; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate; AP1, activator protein1; AQP, acquaporin; BBB, blood-brain barrier; BDNF, brain-derived growth factor; bFGF, basic fibroblast growth factor; bHLH, basic helix loop helix; BMP, bone morphogenetic protein; CNS, central nervous system; CNTF, ciliary neurotrophic factor;COX-2, cyclooxigenase-2; CREB, cAMP response element binding; CSPGs, chondroitinsulphate proteoglycans; ERK, extracellular signal-regulated kinase; EGF, epidermal growth factor; Eph4A, ephrin 4A; Epo, erythropoietin; ET1, Endothelin 1; ET-R, endothelin receptor; GABA, gamma-aminobutyric acid; GDNF, glial cell-line derived neurotropic factor; GF, growth factor; GFAP, glial fibrillary acidic protein; GLAST, glutamate aspartate transporter; GLT1, glutamate transporter 1; GS, glutamine synthase; IFN , interferon-beta; IFNγ, interferon gamma; IGF1, insulin growth factor1; IL1β, interleukin 1 beta; IL2, interleukin 2; IL6, interleukin 6; IL10, interleukin 10; JAK, Janus protein tyrosine kinases; Lcn2, Lipocalin 2; MAPK, mitogen-activated protein kinase; MMP, matrix metalloprotease; mTOR, mammalian target of rapamycin; NFAT, nuclear factor of activated T cell; NFkB, nuclear factor kappa B; NGF, nerve growth factor; NT3, neurotrophin 3; p38MAPK, p38 mitogen-activated protein kinase; PTEN, phosphatase and tensin homolog; SOCS, suppressor of cytokine signaling; SOD, superoxide dismutase; STAT, signal transducers and activators of transcription; TGFα, transforming growth factor alpha;TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha; VCAM1, vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor. Page 4 of 63A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 4...

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“…Genotyping was performed as described previously (Takebayashi et al, 2002b;Tatsumi et al, 2008). Fertilized chick eggs were purchased from Yamagishi Corporation (Mie, Japan) and were incubated at 37°C.…”

Section: Animals and Tissue Preparationmentioning

confidence: 99%

Development of the prethalamus is crucial for thalamocortical projection formation and is regulated by Olig2

et al. 2014

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Thalamocortical axons (TCAs) pass through the prethalamus in the first step of their neural circuit formation. Although it has been supposed that the prethalamus is an intermediate target for thalamocortical projection formation, much less is known about the molecular mechanisms of this targeting. Here, we demonstrated the functional implications of the prethalamus in the formation of this neural circuit. We show that Olig2 transcription factor, which is expressed in the ventricular zone (VZ) of prosomere 3, regulates prethalamus formation, and loss of Olig2 results in reduced prethalamus size in early development, which is accompanied by expansion of the thalamic eminence (TE). Extension of TCAs is disorganized in the Olig2-KO dorsal thalamus, and initial elongation of TCAs is retarded in the Olig2-KO forebrain. Microarray analysis demonstrated upregulation of several axon guidance molecules, including Epha3 and Epha5, in the Olig2-KO basal forebrain. In situ hybridization showed that the prethalamus in the wild type excluded the expression of Epha3 and Epha5, whereas loss of Olig2 resulted in reduction of this Ephas-negative area and the corresponding expansion of the Ephas-positive TE. Dissociated cultures of thalamic progenitor cells demonstrated that substrate-bound EphA3 suppresses neurite extension from dorsal thalamic neurons. These results indicate that Olig2 is involved in correct formation of the prethalamus, which leads to exclusion of the EphA3-expressing region and is crucial for proper TCA formation. Our observation is the first report showing the molecular mechanisms underlying how the prethalamus acts on initial thalamocortical projection formation.

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Genetic fate mapping of Olig2 progenitors in the injured adult cerebral cortex reveals preferential differentiation into astrocytes

Cited by 108 publications

References 51 publications

Differential and cooperative actions of Olig1 and Olig2 transcription factors on immature proliferating cells after contusive spinal cord injury

Differential and cooperative actions of Olig1 and Olig2 transcription factors on immature proliferating cells after contusive spinal cord injury

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Development of the prethalamus is crucial for thalamocortical projection formation and is regulated by Olig2

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