Ciliary Neurotrophic Factor Activates JAK/Stat Signal Transduction Cascade and Induces Transcriptional Expression of Glial Fibrillary Acidic Protein in Glial Cells

Kahn, M.A.; Huang, Chang Jen; Caruso, Angela; Barresi, Vincenza; Nazarian, Ramin; Condorelli, D. F.; Vellis, Jean de

doi:10.1046/j.1471-4159.1997.68041413.x

Cited by 93 publications

(52 citation statements)

References 29 publications

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“…The mechanism of gradual downregulation of ESET during development remains to be determined, but both extrinsic and intrinsic factors could be involved. It was reported that some extrinsic factors such as ciliary neurotrophic factors, leukemia inhibitory factor and cardiotrophin 1 promote astrocyte differentiation (Kahn et al, 1997;Nakashima et al, 1999;Miller and Gauthier, 2007), and these factors could lead to downregulation of ESET expression. It was previously reported that the bHLH genes Hes1 and Ngn2 are expressed in an oscillatory manner in NPCs (Shimojo et al, 2008), and it has been proposed that this oscillation is one of the internal clock mechanisms (Kageyama et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Essential roles of the histone methyltransferase ESET in the epigenetic control of neural progenitor cells during development

et al. 2012

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SUMMARYIn the developing brain, neural progenitor cells switch differentiation competency by changing gene expression profiles that are governed partly by epigenetic control, such as histone modification, although the precise mechanism is unknown. Here we found that ESET (Setdb1), a histone H3 Lys9 (H3K9) methyltransferase, is highly expressed at early stages of mouse brain development but downregulated over time, and that ablation of ESET leads to decreased H3K9 trimethylation and the misregulation of genes, resulting in severe brain defects and early lethality. In the mutant brain, endogenous retrotransposons were derepressed and nonneural gene expression was activated. Furthermore, early neurogenesis was severely impaired, whereas astrocyte formation was enhanced. We conclude that there is an epigenetic role of ESET in the temporal and tissue-specific gene expression that results in proper control of brain development. RESEARCH ARTICLE ESET in neural development MATERIALS AND METHODS Mouse linesESET flox (f) (Matsui et al., 2010), Emx2-Cre (Kimura et al., 2005) and Nes-Cre (Isaka et al., 1999) mice were described previously. Emx2-Cre;ESET(f/+) or Nes-Cre;ESET(f/+) male mice were crossed with ESET(f/f) female mice, and the day when a vaginal plug was observed was scored as embryonic day (E) 0.5. In situ hybridization, immunohistochemistry and antibodiesEmbryos were dissected, fixed in 4% paraformaldehyde (PFA)/PBS overnight and cryoprotected with 20% sucrose for at least 10 hours. On the following day, embryos were embedded in OCT compound (Tissue-Tek) and frozen at -80°C. Fixed samples were sectioned at 16 m with a cryostat and dried for 2 hours. In situ hybridization was then performed as previously described (Imayoshi et al., 2008). Primers used to produce in situ hybridization probes are listed in supplementary material Table S1. For immunohistochemistry, embryos at different ages were fixed in 4% PFA for 2 hours, equilibrated and sectioned as described above. Sections were blocked with 5% normal goat serum or donkey serum in 0.1% Triton X-100/PBS and incubated with primary antibodies at 4°C overnight. The following primary antibodies were used:

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Section: Discussionmentioning

confidence: 99%

Essential roles of the histone methyltransferase ESET in the epigenetic control of neural progenitor cells during development

et al. 2012

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“…In CG-4, CNTF and LIF have been shown to enhance the survival of trophically deprived OL-like cells (Kahn and De Vellis, 1994). The signal transduction pathways activated by CNTF in both primary OL and CG-4 also appear to be similar, as both lead to the activation of JAK/stat signalling cascades (Kahn et al, 1997;Dell'Albani et al, 1998).…”

Section: A Comparison Of Primary Ol and Cg-4mentioning

confidence: 99%

“…Studies on primary cultures of O2A have shown that CNTF and LIF can induce conversion of O2A into astrocytes, as has been assessed by GFAP staining (Hughes et al, 1988;Lillien et al, 1990;Mayer et al, 1994;Gard et al, 1995a,b). Studies conducted on CG-4 also indicate a role for CNTF and LIF in the differentiation of progenitor cells towards astrocytes (Kahn and De Vellis, 1994;Kahn et al, 1997). Furthermore, CNTF and LIF are well known OL survival factors: CNTF has been shown to enhance OL survival after TNF-a treatment or removal of trophic factors, and LIF has also been shown to promote OL survival in vitro (Barres et al, 1993;Louis et al, 1993;Mayer et al, 1994;D.…”

Section: A Comparison Of Primary Ol and Cg-4mentioning

confidence: 99%

Mitogen‐activated protein kinase signalling in oligodendrocytes: a comparison of primary cultures and CG‐4

Stariha¹,

Kim²

2001

Intl J of Devlp Neuroscience

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Oligodendrocytes play a significant role in the central nervous system, as these cells are responsible for myelinating axons and allowing for the efficient conduction of nerve impulses. Therefore, any understanding we can gain about the functional biology of oligodendrocytes will give us important insights into demyelinating diseases such as multiple sclerosis, where oligodendrocytes and myelin are damaged or destroyed. Currently, much attention has focussed on the role of a family of mitogen-activated protein kinases in OL. This kinase family includes the extracellular signal-regulated protein kinases (ERKs), the stress-activated c-Jun N-terminal kinase (JNK), and the 38 kDa high osmolarity glycerol response kinase (p38). The actions of mitogen-activated protein kinases in oligodendrocytes appear to range from proliferation and cell survival to differentiation and cell death. In the past, studies on oligodendrocytes have been hampered by the difficulties inherent in producing large enough quantities of these cells for experimentation. This problem arises in large part due to the post-mitotic nature of mature oligodendrocytes. Over the years, a cell line known as Central Glia-4 (CG-4) has become a popular oligodendrocyte model due to its potentially unlimited capacity for self-renewal. In this review, we will look at the suitability of the Central Glia-4 cell line as an oligodendrocyte model, specifically in respect to studies on mitogen-activated protein kinase signalling in oligodendrocytes.

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“…Moreover, IL1, IL2, IFN , TNF TGF and others have been found to give rise to massive astrogliosis when injected directly into the brain or overexpressed in transgenic animals [37,38,39]. Similarly, ciliary neurotrophic factor (CNTF), a member of the IL6 family of cytokines with growth factor properties, can promote astrogliosis both in vitro [40] and after administration to the intact brain in vivo [41]. Some reactive traits together with progenitor features are also induced by the mitogen TGF [42,43].…”

Section: Cytokines and Growth Factorsmentioning

confidence: 99%

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

Buffo

Rolando

Ceruti

2010

Biochemical Pharmacology

288

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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Ciliary Neurotrophic Factor Activates JAK/Stat Signal Transduction Cascade and Induces Transcriptional Expression of Glial Fibrillary Acidic Protein in Glial Cells

Cited by 93 publications

References 29 publications

Essential roles of the histone methyltransferase ESET in the epigenetic control of neural progenitor cells during development

Essential roles of the histone methyltransferase ESET in the epigenetic control of neural progenitor cells during development

Mitogen‐activated protein kinase signalling in oligodendrocytes: a comparison of primary cultures and CG‐4

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

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