ライフサイエンスコーパス: astrocyte

1 own to be neuroprotective and is released by astrocytes.

2 with the promotion of disease progression by astrocytes.

3 of IL6 and IL8, but not that of CCL5 in SVG astrocytes.

4 ects of kainate-induced seizures on cortical astrocytes.

5 m dendrites and reduced numbers of activated astrocytes.

6 eurons are generated by direct conversion of astrocytes.

7 uroprogenitors give rise to both neurons and astrocytes.

8 loads in neurons and, surprisingly, adjacent astrocytes.

9 c mice expressing GFP and MrgA1 receptors in astrocytes.

10 st in neurons but, surprisingly, in adjacent astrocytes.

11 e in ubiquitinated proteins in MG132-treated astrocytes.

12 ameliorated calcium overload in neurons and astrocytes.

13 h, and this is reduced with SREBP2 knockdown astrocytes.

14 represented by different genes from those in astrocytes.

15 ecreased secretion of exosomes from cultured astrocytes.

16 nal cord, where it is predominantly found in astrocytes.

17 in pHi later during MAc in both neurons and astrocytes.

18 rvous system (CNS) myelin are contributed by astrocytes.

19 voked by paracrine signals from iron-starved astrocytes.

20 elease of organic osmolytes from primary rat astrocytes.

21 from the coordinated activity of neurons and astrocytes.

22 ll-to-cell communication between neurons and astrocytes.

23 ordings confirmed EAAT2 is functional on nTS astrocytes.

24 e latter increase was predominantly found in astrocytes.

25 re, we investigated the impact of AbetaOs in astrocytes, a less known subject.

26 ouse models demonstrated that dysfunction of astrocytes, a major type of glial cell, leads to neurona

27 By demonstrating that AbetaOs decrease astrocyte ability to protect synapses, our results unrav

28 Within 24 hours of IL1beta induction, astrocytes acquired reactive characteristics.

29 ic activation in the ischemic brain and that astrocytes activated by neuronal uPA promote synaptic re

30 The results suggest that astrocyte activation drives hyperexcitability during AD

31 Notably, astrocyte activation in pFRG/RTN triggered local PGE2 re

32 Therefore, we conclude that astrocyte activity determines fear responses by selectiv

33 The accumulation of alpha-SYN in the astrocytes affects their lysosomal machinery and induces

34 ogenous neural stem cells or neuroprotective astrocytes after SCI.

35 hway is disrupted in human stem cell derived astrocyte and mouse models of amyotrophic lateral sclero

36 dual neurons can be excited by more than one astrocyte and that individual astrocytes may determine a

37 e, an essential energy substrate produced by astrocytes and critical for memory formation, decreases

38 OB, we observed activation of microglia and astrocytes and decreased expression of tyrosine hydroxyl

39 As both astrocytes and DISC1 influence adult neurogenesis in the

40 ervous system, apoE is produced primarily by astrocytes and functions in transporting lipids includin

41 le in the development of PD are expressed in astrocytes and have important roles in astrocyte functio

42 ctivation also regulates glutamate uptake in astrocytes and how this shapes excitatory synaptic trans

43 tic activation mediates a cross talk between astrocytes and injured neurons that promotes synaptic re

44 nges after aseptic trauma in mice related to astrocytes and later in neurons that emphasize the role

45 n-film probes yield a marked accumulation of astrocytes and microglia and decrease of neurons for the

46 Infected mixed primary cultures of astrocytes and microglia had higher levels of MMP2 and M

47 spond differently to photo-toxicity, in that astrocytes and microglia undergo morphological changes,

48 rt findings on the bioenergetic interplay of astrocytes and neurons and discuss how dysregulation of

49 Fast and reciprocal communication between astrocytes and neurons is enabled by a diverse set of me

50 ifferences in their relative weights between astrocytes and neurons.

51 d minimal overlap between CREB signatures in astrocytes and neurons.

52 IB expression was predominantly localized to astrocytes and neurons.

53 ven when mutant protein is expressed only in astrocytes and not in neurons.

54 letion of the same gene in astrocytes, or in astrocytes and oligodendrocytes, caused a persistent hyp

55 ies, as well as the subsequent generation of astrocytes and oligodendrocytes.

56 A expression was more frequently observed in astrocytes and oligodendroglia, whereas NFIB expression

57 Our data reveal that despite expression on astrocytes and other cells types in the brain, ADAM17 up

58 n-3 PUFAs markedly inhibit the activation of astrocytes and protect the AQP4 polarization in the affe

59 y, we utilized the close interaction between astrocytes and retinal ganglion cells (RGCs) in the eye

60 gaps in our knowledge of the cell biology of astrocytes and the mechanisms they use to interact with

61 in various cell types, including microglia, astrocytes and vascular endothelial cells.

62 ed with human brain endothelial cells, human astrocytes, and human brain pericytes in mono-, co-, and

63 barrier (BBB) consists of endothelial cells, astrocytes, and pericytes embedded in basal lamina (BL).

64 ught to investigate the impact of AbetaOs on astrocytes, and to determine whether this impact is rela

65 olytic and acetate metabolism in neurons and astrocytes, and ultimately synaptic plasticity loss evid

66 udy we investigate the possible link between astrocyte arbors and presence of OPMs.

67 Astrocytes are a primary defense against hyperexcitabili

68 Astrocytes are abundant within mature neural circuits an

69 Transcriptional changes in astrocytes are accompanied by alterations in phagocytic

70 In contrast, SCN astrocytes are active during circadian nighttime, when t

71 oglia, innate immune cells of the brain, and astrocytes are also critical contributors to masculiniza

72 Astrocytes are an abundant and evolutionarily conserved

73 Human astrocytes are increasingly appreciated as important con

74 Astrocytes are key players in the pathology of multiple

75 been fully tested, and the possibility that astrocytes are neural circuit specialized remains largel

76 confirm that plaque-localised microglia and astrocytes are reduced in ABX-exposed mice.

77 Reactive astrocytes are strongly induced by central nervous syste

78 Astrocytes are the most populous glial subtype and are c

79 Here, we demonstrate that pFRG/RTN astrocytes are the PGE2 source.

80 Astrocytes are the primary support cells of the CNS and

81 st, the gene networks coordinated by CREB in astrocytes are unknown despite the fact that the astrocy

82 These findings highlight astrocytes as a critical component of the neural systems

83 ranscriptional programs regulated by CREB in astrocytes as compared to neurons using, as study materi

84 dentified the protective factors released by astrocytes as insulin and insulin-like growth factor-1 (

85 later in neurons that emphasize the role of astrocytes as key intermediaries between peripheral immu

86 Taken together, our data identify cerebellar astrocytes as key responders to viral infection and high

87 rding astrocyte glutamate release as well as astrocyte association with synapses with respect to the

88 survival protein, phosphoprotein enriched in astrocytes at approximately 15 kDa (PEA15), and its mRNA

89 aining a better understanding of the role of astrocytes at synapses in health and disease will provid

90 It is predominantly expressed in astrocytes at the blood-brain and blood-liquor interface

91 ies have revealed the presence of "glia" or "astrocytes" at the nodes.

92 Blockade of vesicular exocytosis in preBotC astrocytes bilaterally (using an adenoviral vector to sp

93 e network excitability involve, for example, astrocyte Ca(2+) and Na(+) signalling, K(+) buffering, g

94 ced a long-lasting reduction in resting free astrocyte Ca(2+) and that this phenomenon changed arteri

95 However, whether resting astrocyte Ca(2+) can adjust to a new steady-state level,

96 screpancy, we examined a different aspect of astrocyte Ca(2+): the resting, steady-state free Ca(2+)

97 The results confirm that astrocytes can act as excitatory nodes that can influenc

98 Astrocytes can control many aspects of neuronal function

99 Furthermore, iPSC-derived astrocytes can replicate prions associated with the majo

100 d a stem cell model of FTD to examine if FTD astrocytes carry an intrinsic propensity to degeneration

101 Briefly, stable astrocytes clones with an integrated fluorescent HIV rep

102 tern of ribosome-associated mRNA profiles in astrocytes closely follows the dorsoventral axis, especi

103 These findings suggest a new type of neuron-astrocyte communication, based on the expression of AE3

104 Astrocytes comprise half of the cells in the brain.

105 We found that astrocyte conditioned medium (ACM) applied directly to t

106 ed neuroprotective signal present in retinal astrocyte conditioned medium (ACM).

107 sed on SOX9 immunolabeling, we document that astrocytes constitute a smaller fraction of total cell n

108 Astrocytes constitute approximately 30% of the cells in

109 Supernatants from rPrP(c)-treated astrocytes containing factors produced in response to th

110 die after axotomy, strongly suggest that A1 astrocytes contribute to the death of neurons and oligod

111 insic influences, such as those arising from astrocytes, contribute to motor neuron malfunction and l

112 L2, and NL3, which are expressed by cortical astrocytes, control astrocyte morphogenesis through inte

113 sychiatric genetic risk factors expressed in astrocytes could affect adult hippocampal neurogenesis a

114 te and potassium buffering capacity, loss of astrocyte coupling, and changes in cell morphology.

115 unction for uPA-uPAR as mediator of a neuron-astrocyte cross talk that promotes synaptic recovery in

116 Studies of neuronal and astrocyte cultures and a computational analysis of SCI R

117 dant) in TDP-43M337V patient fibroblasts and astrocyte cultures from TDP-43Q331K mice, indicative of

118 subpassage of prions from infected to naive astrocyte cultures, indicating the generation of prion i

119 accumulated ssDNA present in the neuron and astrocyte cytoplasm of TREX1 mutated stem cell-derived o

120 risk factor for demyelination resulting from astrocyte death, which leads to microglial activation, b

121 ethylation inhibitor 5-azacytidine, enforces astrocyte dedifferentiation.

122 Following spinal cord injury (SCI), astrocytes demonstrate long-lasting reactive changes, wh

123 Astrocytes depressed excitatory synapses from basolatera

124 s issue of JEM, Krejciova et al. report that astrocytes derived from human iPSCs can replicate human

125 btypes coupled with different K(+) channels, astrocyte-derived ATP differentially modulates the excit

126 inst synaptotoxic AbetaOs can be mediated by astrocyte-derived insulin/IGF1, but that this protection

127 AxD is a primary astrocyte disease because GFAP expression is specific to

128 database resources and approaches to explore astrocyte diversity and function throughout the adult br

129 istent hypomyelination, as did deletion from astrocytes during postnatal development.

130 is caused by the loss of motor neurons, but astrocyte dysfunction also contributes to the disease in

131 Our data suggest a role for astrocyte dysfunction in neurological disease and identi

132 neurons downregulated d-serine levels, while astrocytes enhanced production and release of d-serine.

133 cellular lactate, those with only SOD1(G93A) astrocytes exhibited the reverse.

134 study materials, transcriptome databases of astrocyte exposed to well-known activators of CREB-depen

135 Here we show that selective stimulation of astrocytes expressing channelrhodopsin-2 in the CA1 area

136 Astrocytes extend highly branched processes that form fu

137 raft, no axons exited, and Schwann cells and astrocytes failed to integrate.

138 Neurons cultivated in the absence of an astrocyte feeder layer showed abundant AbetaO binding to

139 ulate or measure flux of internal calcium in astrocytes, focusing on G protein-coupled receptor-media

140 n immediate, but transient, vacuolization of astrocytes, followed over several days by astrogliosis.

141 suggest yet unexplored functions of newborn astrocytes for the aging hippocampal circuitry.

142 Despite the clear importance of astrocytes for the establishment and maintenance of prop

143 nstrate the importance of another cell type, astrocytes, for biological timekeeping.

144 These active astrocytes formed a subnetwork within the respiratory ne

145 uced an unexpected long-lasting reduction in astrocyte free Ca(2+) in the soma and endfeet.

146 In astrocytes from animals that lived in an enriched enviro

147 oped a system combining cortical neurons and astrocytes from closely related species, followed by RNA

148 stence of distinct innate immune programs in astrocytes from evolutionarily disparate regions of the

149 gate the metabolic effects of NO in cultured astrocytes from mice by taking advantage of the high spa

150 endothelial cell proliferation but protects astrocytes from oxidative stress.

151 The top gene pathways that were changed in astrocytes from spinal cord during chronic EAE involved

152 between neuroanatomic regions when comparing astrocytes from spinal cord, cerebellum, cerebral cortex

153 hat the in vitro half-lives of total GFAP in astrocytes from wild-type and mutant mice were similar a

154 ed in astrocytes and have important roles in astrocyte function.

155 Astrocytes functionally interact with neurons, but their

156 orders, has been implicated in regulation of astrocyte functions.

157 However, the dynamics of neuron and astrocyte generation throughout adulthood has not been s

158 Further, I compile evidence regarding astrocyte glutamate release as well as astrocyte associa

159 In particular, SMN-deficient astrocytes have decreased levels of monocyte chemoactive

160 The discovery that astrocytes have different types of reactive states has i

161 Astrocytes have diverse, remarkably complex shapes in di

162 In vivo, mice with knockout of SREBP2 in astrocytes have impaired brain development and behaviora

163 tightly bundled chains within a meshwork of astrocytes; however, the cell-cell cues that organize th

164 ging and was instead upregulated by reactive astrocytes in a number of settings, including a murine m

165 Additional exploration of astrocytes in HD mouse models and humans is needed and m

166 ally relevant models for investigating human astrocytes in health and disease.

167 cular unit endothelial cells and to reactive astrocytes in mouse models of AD.

168 This review discusses the role of astrocytes in neurovascular signalling in both physiolog

169 -selective roles of cortical and subcortical astrocytes in regulating cortical or subcortical neurona

170 future experiments to explore the nature of astrocytes in situ.

171 ty, and re-established perivascular end-feet astrocytes in symptomatic ALS mice may represent BSCB re

172 Given the key roles of astrocytes in synapse formation, plasticity, and functio

173 that SOX9 is almost exclusively expressed by astrocytes in the adult brain except for ependymal cells

174 sease because GFAP expression is specific to astrocytes in the central nervous system (CNS).

175 HIV reservoirs in the human body, including astrocytes in the human brain.

176 of Scofield et al., who explored the role of astrocytes in the nucleus accumbens in the neural mechan

177 S cell-derived NPCs to elucidate the role of astrocytes in the pathogenesis of FTD.

178 d in misaligned neuroblasts and disorganized astrocytes in the RMS/SVZ, linking EphA4 forward signali

179 dies have examined the influence of reactive astrocytes in the tripartite synapse following TBI.

180 scular unit, including endothelial cells and astrocytes, in mouse models of AD.

181 nts of GFAP causes many molecular changes in astrocytes, including proteasome inhibition, stress kina

182 IL-1beta-positive astrocytes increased in the Tg(CJD) hippocampus, and blo

183 In contrast, we found that SMA astrocytes increased microRNA (miR) production and secre

184 cids in cell culture, using primary cortical astrocytes, indicated that the in vitro half-lives of to

185 plications for mechanisms of seizure-induced astrocyte injury and potential therapeutic applications

186 way is involved in mediating seizure-induced astrocyte injury.

187 vo molecular and functional heterogeneity of astrocytes inter-regionally from adult brain.

188 ne, which is the gene that encodes the major astrocyte intermediate filament protein.

189 n vivo is prevented when the formation of A1 astrocytes is blocked.

190 oxide dismutase 1 (SOD1(G93A)) expression in astrocytes is selectively toxic to motor neurons in co-c

191 A typical feature of astrocytes is their high expression level of connexin43

192 +): the resting, steady-state free Ca(2+) of astrocytes, its modulation, and its potential role in th

193 ivity of V1 neurons is given as input to the astrocyte layer.

194 sential clock gene Bmal1 specifically in SCN astrocytes lengthened the circadian period of clock gene

195 n expression in glutamine synthetase (GS) in astrocyte-like glia and in changes in the gap-junction c

196 re the authors describe the morphogenesis of astrocyte-like glia in the Drosophila optic lobe, and th

197 found that in the Drosophila visual system, astrocyte-like medulla neuropil glia (mng) variants acqu

198 elated to cell differentiation, particularly astrocyte lineage genes, were upregulated in KO cells.

199 Computational analyses indicate that astrocyte-localized translation is both sequence-depende

200 Mature astrocyte markers first appeared after 6 months, while m

201 more than one astrocyte and that individual astrocytes may determine a neuron's synchronized network

202 This suggests that reactive astrocytes may not be the main CSPG contributory factor

203 of miR-146a may be a contributing factor in astrocyte-mediated SMA pathology.

204 hat AE3 (present in hippocampal neurons, not astrocytes; mediates HCO3(-) efflux) enhances intracellu

205 electronics showed that the distribution of astrocytes, microglia, and neurons became uniform from 2

206 Here we show that astrocyte morphogenesis in the mouse cortex depends on d

207 re expressed by cortical astrocytes, control astrocyte morphogenesis through interactions with neuron

208 mechanisms that control the establishment of astrocyte morphology are unknown, and it is unclear whet

209 1(G93A) cell types highlight the role of the astrocyte-motor neuron interaction in the resulting meta

210 Mechanisms of astrocyte-neuron interactions that can quickly increase

211 However, rapid changes of astrocyte neurotransmitter uptake and morphology may als

212 We have been studying the astrocytes of Alexander disease (AxD), which is caused b

213 e JCI, Horng and colleagues demonstrate that astrocytes of the glia limitans induce tight junction fo

214 from astrocyte-spinal neuron co-cultures and astrocyte-only cultures.

215 eraction is functional in LUAD and show that astrocytes oppose brain metastasis by mediating the down

216 ntly, embryonic deletion of the same gene in astrocytes, or in astrocytes and oligodendrocytes, cause

217 rotective and anti-inflammatory signature in astrocytes, partially linked to the STAT3 network.

218 Astrocytes perform critical non-cell autonomous roles fo

219 rovascular unit (NVU) that includes neurons, astrocytes, pericytes, and microglia as well as the bloo

220 for pathways consistent with known roles for astrocyte processes, such as GABA and glutamate metaboli

221 of the nodes in all three regions contained astrocyte processes, while 33-49% of nodes contained NG2

222 e transcripts that are locally translated in astrocyte processes.

223 synthesis occurs within distal, perisynaptic astrocyte processes.

224 Astrocytes produce and supply metabolic substrates to ne

225 trained wild-type mice were able to increase astrocyte-produced glial fibrillary acidic protein in th

226 Together, these data indicate that altered astrocyte production of miR-146a may be a contributing f

227 We thus report core astrocyte properties, reveal evidence for specialized as

228 ise the possibility that local production of astrocyte proteins may support microscale alterations of

229 The reprogramming efficiency of human astrocytes reaches up to 16%, resulting in iDANs with ap

230 We found that neurons release uPA and astrocytes recruit uPAR to their plasma membrane during

231 idated in vivo, where deletion of trkB.T1 in astrocytes reduced cell proliferation and migration.

232 fically express tetanus toxin light chain in astrocytes) reduced the HVR in anaesthetized rats, indic

233 demonstrated that type I IFNAR signaling in astrocytes regulates BBB permeability and protects the c

234 In contrast, control-derived astrocytes rescued the morphological neuronal phenotype

235 ions on ingrowing blood vessels and reactive astrocytes, respectively.

236 Astrocyte responds to neuronal activity with calcium wav

237 K1epsilon tau mutation specifically from SCN astrocytes resulted in lengthened rhythms in the SCN and

238 terestingly, co-culture experiments with FTD astrocytes revealed increased oxidative stress and robus

239 ompartments: (a) non-neural lesion core, (b) astrocyte scar border, and (c) surrounding spared but re

240 We found that human iPSC-derived astrocytes secreted abundant apoE with apoE4 lipoprotein

241 Overall, our work demonstrates that astrocyte-secreted factors alter migration and morpholog

242 Astrocyte-secreted glypican 4 induces formation of activ

243 Interestingly, cortical or subcortical astrocytes selectively promote neurite growth and synapt

244 However, Scube2, a glycoprotein regulating astrocyte Shh release was decreased, inhibiting Shh deli

245 Ex vivo studies with hypothalamus-derived astrocytes showed that LPL expression is upregulated by

246 Astrocytes slowly migrated from grafts.

247 Astrocyte-specific elimination of the astrocytic d-serin

248 This astrocyte-specific genetic manipulation silenced the wak

249 Mice with astrocyte-specific loss of IFNAR signaling showed decrea

250 deno-associated virus vectors containing the astrocyte-specific promoter Gfa2 and the NFAT inhibitory

251 After SCI, astrocyte-specific trkB.T1 KO mice showed reduced hyperp

252 lysis by (1)H NMR spectroscopy of media from astrocyte-spinal neuron co-cultures and astrocyte-only c

253 To examine metabolic changes in astrocyte-spinal neuron co-cultures, we carried out meta

254 e pathological states.SIGNIFICANCE STATEMENT Astrocytes spontaneously release glutamate (Glut) and ot

255 Astrocytes spontaneously release glutamate (Glut) as a g

256 Two distinct astrocyte subtypes were found using transgenic mice expr

257 eal a variety of structural abnormalities in astrocytes, such as vacuolization and astrogliosis.

258 production and secretion compared to control astrocytes, suggesting potential toxic gain-of-function

259 bellar astrocytes than did cerebral cortical astrocytes, suggesting that IFNAR signaling has brain re

260 ible for relapse vulnerability take place in astrocyte systems that regulate glutamate uptake and rel

261 ced expression in human and mouse cerebellar astrocytes than did cerebral cortical astrocytes, sugges

262 thwhile to identify defects in SMN-deficient astrocytes that compromise normal function.

263 bolic, structural, and functional changes in astrocytes that lead to a disruption of the neuroglial m

264 majority of newly proliferated scar-forming astrocytes that protect tissue and function after spinal

265 By simply varying the radius of the astrocytes, the extent of lateral excitatory neuronal co

266 Astrocytes, the most abundant glial cells in the mammali

267 In astrocytes, the top triad of functions regulated by CREB

268 ed motor neurons, which in turn can activate astrocytes through ephrin-B1-mediated stimulation of sig

269 Functionally, myelin debris was taken up by astrocytes through receptor-mediated endocytosis and res

270 NS in all mice tested and initially targeted astrocytes throughout the brain.

271 sions, a second barrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctiona

272 atched cocultures, exhibiting region-matched astrocyte to neuron communication.

273 exosomal microRNA (miRNA-142-3p) from brain astrocytes to cancer cells.

274 duces the expression of alphaB-crystallin in astrocytes to decrease exosome secretion in the HD brain

275 s study raise the prospect of using modified astrocytes to improve the survival, maturation, and inte

276 For experimental exposure of astrocytes to variant CJD (vCJD), the kinetics of prion

277 Activation of exogenous MrgA1Rs expressed in astrocytes tripled astrocytic calcium oscillation freque

278 We conclude that astrocytes tune the gating of synaptic NMDARs to the vig

279 results generated new molecular signature of astrocyte types in the adult CNS, providing insights int

280 Astrocytes undergo important phenotypic changes in many

281 the plasma membrane, are also released from astrocytes via exocytotic secretion.

282 ty of Cx43 hemichannels recorded in cultured astrocytes was [Ca(2+)]I dependent.

283 although repopulation of the lesion site by astrocytes was delayed significantly.

284 enes while immune pathway gene expression in astrocytes was increased.

285 The neuroprotective potential of astrocytes was itself sensitive to chronic AbetaO exposu

286 population of the optic nerve lesion site by astrocytes was significantly delayed upon microglia depl

287 into OAPs and its role in the regulation of astrocyte water homeostasis have been studied.

288 , aggregation, and role in the regulation of astrocyte water homeostasis of the newly described water

289 virtual absence of ER-localized ClC-4 in WT astrocytes, we performed association studies by high-res

290 ulated by Mtb-stimulation, but Shh levels in astrocytes were unchanged.

291 rP(c) decreased uptake of this metabolite in astrocytes, which could lead to neurotoxicity and neuron

292 Here we show that a subtype of reactive astrocytes, which we termed A1, is induced by classicall

293 The spheroid core is comprised mainly of astrocytes, while brain endothelial cells and pericytes

294 Here we show that coculture of control astrocytes with neurons enhances neurite outgrowth, and

295 inflammatory mediators, because treatment of astrocytes with rPrP(c) increased secretion of CCL2, CXC

296 ones, which provide brain cells (neurons and astrocytes) with an energy source that is more efficient

297 properties, reveal evidence for specialized astrocytes within neural circuits, and provide new, inte

298 Here, we demonstrated that daily rhythms in astrocytes within the mammalian master circadian pacemak

299 inus-truncated human DISC1 (mutant DISC1) in astrocytes would affect adult hippocampal neurogenesis a

300 Coculturing endothelial cells with astrocytes yielded the greatest resistance over time.