ライフサイエンスコーパス: astroglial

1 Because astroglial A2AR regulate the availability of glutamate,

2 e nervous system disease caused by a primary astroglial abnormality, to perform an in vivo screen of

3 , demyelination, macrophage recruitment, and astroglial activation and proliferation.

4 ochemical evaluation revealed microglial and astroglial activation as well as neuronal cell loss in e

5 These findings provide evidence of astroglial activation by tissue injury, concomitant IL-1

6 Vigilance-dependent astroglial activation is abolished by deletion of alpha(

7 t the retinas of tg7 and tgNSE mice both had astroglial activation with increased chemokine expressio

8 enuated MPTP-induced striatal microglial and astroglial activation.

9 re accompanied by state-dependent changes in astroglial activity.

10 Astroglial alpha-synuclein-positive cytoplasmic accumula

11 criptional activation and is responsible for astroglial alterations in neural injury.

12 white matter were also the progeny of GFAP+ astroglial ancestors.

13 enes was abolished in Act1-deficient primary astroglial and gut epithelial cells.

14 phic growth factor release and decreased the astroglial and microglial activation induced by DSS.

15 (superoxide dismutase-2), neuroinflammation (astroglial and microglial activation), neurogenesis (Brd

16 creased dendritic arborizations, and reduced astroglial and microglial activation, as well as improve

17 Astroglial and microglial activation, reduced neuronal d

18 hypersensitivity caused by augmented spinal astroglial and microglial activity.

19 induced cytokine protein release in primary astroglial and microglial cell cultures.

20 These changes were accompanied by increased astroglial and microglial reactivity, possibly as a resp

21 Each lesion type displayed unique astroglial and microglial responses that corresponded to

22 Our observations establish that the astroglial and neurofibrillary tau pathologies of CTE ar

23 sides) integrated in the rigid structures of astroglial and neuronal lipid rafts.

24 heir divergent developmental trajectories in astroglial and oligodendroglial lineages.

25 that only PSP-tau and CBD-tau strains induce astroglial and oligodendroglial tau inclusions, recapitu

26 se prodrugs to incorporate into endothelial, astroglial, and neuronal cells according to a structure-

27 he corpus callosum appears to be balanced by astroglial apoptosis, because overall numbers of corpus

28 Ezrin knockdown reduced astroglial association with synapses and potentiated cue

29 f all caliber and putative smooth muscle and astroglial basement membrane compartments.

30 line showed early transient increases of the astroglial biomarkers S-100B and glial fibrillary acidic

31 tile niche at the lesion site incurs massive astroglial but not neuronal differentiation of NSCs.

32 indicate that Olig2-expressing cells in the astroglial but not the oligodendroglial lineage are the

33 co-cultures, we demonstrate that the loss of astroglial (but not neuronal) FMRP particularly reduces

34 in vivo imaging, we show in Drosophila that astroglial Ca(2+) signaling increases with sleep need.

35 These findings define astroglial Ca(2+) signaling mechanisms encoding sleep ne

36 Astroglial [Ca(2+)](i) responses are triggered by transm

37 It was found that astroglial [Ca(2+)]i responses triggered by decreases in

38 Thus, astroglial calcium activity changes dynamically across v

39 We found that astroglial calcium elevations during PIDs are mediated b

40 Together, these data implicate astroglial calcium pathways as potential targets for str

41 ead-fixed, unanesthetized mice, we show that astroglial calcium signals are highest in wake and lowes

42 We also find that astroglial calcium signals during non-rapid eye movement

43 We now report that conditional deletion of astroglial CCL2 significantly decreases CNS accumulation

44 s suggest that therapies designed to inhibit astroglial CCL2-driven trafficking of monocyte-derived m

45 induction appear to play a critical role in astroglial cell activation (astrogliosis) following CNS

46 f progenitor cell proliferation and neuronal/astroglial cell differentiation.

47 Furthermore, using an astroglial cell line, primary culture of astrocytes, and

48 d cell autonomously by CC axons or by the IG astroglial cell lineage, but rather acts non-cell autono

49 cular changes in synaptic protein levels and astroglial cell marker in a region specific manner.

50 lation contributes to the maintenance of the astroglial cell population.

51 We also identified SVG-A astroglial cell-derived cells to be highly permissive fo

52 LTD induction requires CB1R in astroglial cells (but not in GABAergic or glutamatergic

53 e report that exosomes released from retinal astroglial cells (RACs) suppress retinal vessel leakage

54 Astroglial cells also express AMPA receptors, but their

55 progenitors appear to give rise to abnormal astroglial cells and induce periventricular lesions and

56 tentials due to loss of spinal cord neurons, astroglial cells and myelin; urinary incontinence.

57 Consolidated evidence indicates that astroglial cells are critical in the homeostatic regulat

58 ast to exocytosis, the endocytic pathways in astroglial cells are poorly understood.

59 the accumulation of activated microglial and astroglial cells around yeast aggregates, forming fungal

60 keletal dynamics of cortical progenitors and astroglial cells have critical roles in the emergence of

61 These findings suggest a role for astroglial cells in the alteration of circadian timing b

62 the central nervous system, and the role of astroglial cells in this process is increasingly recogni

63 Microglial and astroglial cells play a key role in the development and

64 l stem cells (NSCs), a specialized subset of astroglial cells that are endowed with stem properties a

65 t hypoxic injury increases the proportion of astroglial cells that attain a neuronal fate.

66 e then used human glioma cell lines as model astroglial cells to represent high (T98) and low (A172)

67 SynCAM1 is also expressed in astroglial cells where it mediates astrocyte-to astrocyt

68 ulates translational expression of mGluR5 in astroglial cells, and FMRP-dependent down-regulation of

69 ng Bergmann glia (BG), which are specialized astroglial cells, from the external granule layer to the

70 res, such as capillary-associated pericytes, astroglial cells, leptomeninges, and the choroid plexus.

71 that allows us to trace the progeny of GFAP+ astroglial cells, we show that hypoxic injury increases

72 f at least two distinct heteromeric VRACs in astroglial cells.

73 rminants of transport activity in individual astroglial cells.

74 of FMRP in regulating protein expression in astroglial cells.

75 the effect of pulsed infrared laser light on astroglial cells.

76 greater sensitivity to thiopurine therapy in astroglial cells.

77 n the extensive activation of microglial and astroglial cells.

78 lutamate transporters primarily expressed in astroglial cells.

79 found in areas enriched with microglial and astroglial cells.

80 increased synaptic maturation and number of astroglial cells.

81 The primary progenitors (B1 cells) have astroglial characteristics but retain important neuroepi

82 The growth inhibitions from CNS myelin and astroglial chondroitin sulfate proteoglycans partially a

83 Here, we show that astroglial CNTF expression in the adult mouse striatum i

84 Astroglial CNTF expression was not affected by diffusibl

85 hermore, we demonstrate that aspirin-induced astroglial CNTF was also functionally active and that su

86 rated actions across the oligodendrocyte and astroglial compartments that are at least partially mech

87 ogical tools, we showed that the activity of astroglial connexin 43 hemichannels, opened in an activi

88 Primary astroglial cultures from cKO mice expressed elevated fib

89 the activated state of cerebral endothelium, astroglial Cx43 controls immune recruitment as well as a

90 This work demonstrates that astroglial Cx43 hemichannel activity is associated with

91 However, whether astroglial Cx43 hemichannels are active in resting condi

92 furthermore demonstrate that the activity of astroglial Cx43 hemichannels in resting states regulates

93 Consequently, in the absence of astroglial Cx43, recruited immune cells elaborate a spec

94 rain cause irreversible primary neuronal and astroglial damage associated with terminal dendritic bea

95 In addition, lack of astroglial-derived CCL2 results in increased accumulatio

96 on catalyzed by the enzyme Hs2st, in midline astroglial development and in regulating FGF protein lev

97 al lineage-specific genes, while suppressing astroglial differentiation genes including NFIA.

98 Thus, this new paradigm of human astroglial differentiation is useful for studying the he

99 ymorphonuclear leukocytes) blocked hCNS-SCns astroglial differentiation near the lesion epicenter and

100 of hCNS-SCns at 0 dpi resulted in localized astroglial differentiation of donor cells near the lesio

101 iche for promoting neuronal while inhibiting astroglial differentiation of NSCs is not reported.

102 in Id2(-/-) mutant mice prematurely undergo astroglial differentiation within a disorganized rostral

103 erentiation was accompanied by inhibition of astroglial differentiation.

104 Postmortem quantitative analysis of regional astroglial distribution and morphology based on glial fi

105 vity in VGluT1 KO mice significantly reduces astroglial domain growth and the induction of GLT1 in th

106 lthough accumulating evidence indicates that astroglial dysfunction contributes to motor neuron degen

107 We hypothesized that in HE, astroglial dysfunction could impair metabolic communicat

108 Astroglial dysfunction is known to be present in HE.

109 portance of glial cell pathology, especially astroglial dysfunction, in the pathophysiology of neurop

110 d similar increases in width of perivascular astroglial end-feet in brain.

111 To study astroglial energy metabolism and the directionality of l

112 rized by unmyelinated axons and perisynaptic astroglial envelopes.

113 aves and thereby represent the substrate for astroglial excitability.

114 ATP transmits astroglial excitation to the brainstem respiratory netwo

115 ARACHNE can combine neuronal (wired) and astroglial (extracellular volume-transmission driven) ne

116 , our results demonstrate that Cx43 is a new astroglial factor promoting the immune quiescence of the

117 nsiently altered hNSC migration and reversed astroglial fate after spinal cord injury.

118 structures were used to quantify changes in astroglial fibers in an automated fashion.

119 ic protein demonstrated that SHG arises from astroglial filaments.

120 hese results show that the selective loss of astroglial FMRP contributes to cortical synaptic deficit

121 mpelling evidence that the selective loss of astroglial FMRP contributes to cortical synaptic deficit

122 ed on neurons; whether the selective loss of astroglial FMRP in vivo alters astrocyte functions and c

123 Here we showed that selective loss of astroglial FMRP in vivo up-regulates a brain-enriched mi

124 Although the selective loss of astroglial FMRP only modestly increases spine density an

125 ivo modulation of FXS synaptic phenotypes by astroglial FMRP.

126 aptic elements dynamically coordinate normal astroglial function and also provide a fundamental signa

127 ndicate that disruption of SynCAM1-dependent astroglial function results in behavioral abnormalities

128 This effect of compromised astroglial function was specific to the NTS as expressio

129 brane and calcium stores, and contributes to astroglial function, regulation, and response to mechani

130 How these astroglial functions are regulated, especially by neuron

131 e loss of FMRP alters protein expression and astroglial functions remains essentially unknown.

132 olecular atlas for exploring region-specific astroglial functions.

133 BA), can be released through the reversal of astroglial GABA transporters.

134 9 transcription, suggesting that TNF induces astroglial Gal-9 through the TNF/TNFR1/JNK/cJun signalin

135 Altered expression and function of astroglial gap junction protein connexin 43 (Cx43) has i

136 hy and an increased level of connexin 43, an astroglial gap junction protein.

137 ase of neurodegeneration, a mismatch between astroglial Glu uptake and presynaptic Glu release could

138 8:A > C (g.-181A > C) SNP in the promoter of astroglial glutamate transporter (EAAT2) and the same ap

139 r, compounds that increase expression of the astroglial glutamate transporter GLT-1 (N-acetylcysteine

140 cits in FXS, presumably through dysregulated astroglial glutamate transporter GLT1 and impaired gluta

141 cits in FXS, likely through the dysregulated astroglial glutamate transporter GLT1 expression and imp

142 evidence suggests that abnormalities in the astroglial glutamate transporter localization and functi

143 We found that astroglial glutamate transporter subtype glutamate trans

144 Inducing glutamate spillover by blocking astroglial glutamate transporters (GLT-1) had no effect

145 lso exhibited a progressive depletion of the astroglial glutamate transporters GLT-1 and GLAST.

146 TP induction thus prompts spatial retreat of astroglial glutamate transporters, boosting glutamate sp

147 particularly via expression and function of astroglial glutamate transporters.

148 s been shown that cocaine experience impairs astroglial glutamate uptake and release in the nucleus a

149 (IG), producing a focus of Slit2-expressing astroglial guidepost cells essential for interhemispheri

150 mer disease (AD) brain and to stressed human astroglial (HAG) cells in primary culture.

151 king astroglia-derived Wnt signaling reduces astroglial HIFalpha-regulated CNS angiogenesis.

152 Astroglial homeostatic actions are initiated and control

153 Astroglial homeostatic responses are tightly coordinated

154 ll level, G34R/V tumors harbor dual neuronal/astroglial identity and lack oligodendroglial programs,

155 criminate between genes that function during astroglial immortalization vs. later stages of tumor dev

156 y event during lesion formation and leads to astroglial immune responses.

157 matory infiltrates had subsided, and massive astroglial induction of CCL2 (MCP-1), a chemokine for CC

158 opagated in these mice, which indicates that astroglial infection is sufficient for JCV spread.

159 The levels of the astroglial injury biomarker S-100 calcium-binding protei

160 players is associated with acute axonal and astroglial injury.

161 phic lateral sclerosis all result in reduced astroglial KBBP expression and transcriptional dysfuncti

162 demyelinated area, we observed a decrease of astroglial KIR4.1 but not glial fibrillary acidic protei

163 egulation of neuronal, endothelial, and less astroglial LAT1/LAT2/CD98 amino acid transporter express

164 osons in NSCs induced the immortalization of astroglial-like cells, which were then able to generate

165 ne neural stem cells (NSCs) into neurons and astroglial-like cells.

166 interneurons are produced exclusively by PWM astroglial-like progenitors, whereas PCL precursors prod

167 d (8%) and differentiated along neuronal and astroglial lineages, where improved cognition was associ

168 Moreover, when astroglial lipid synthesis was inhibited, oligodendrocyt

169 creased protein expression for the typically astroglial-localized glutamate transporters in the medio

170 ng K(+)-Cl(-) cotransporter KccB also caused astroglial malformation and paralysis, supporting the id

171 ing events in glioma cell lines and possibly astroglial malignancies.

172 c neuropil territories to form a stereotyped astroglial map.

173 fibrillary acidic protein (GFAP) is the main astroglial marker during astrogliogenesis, but it is als

174 BP and GLAST and later in embryogenesis, the astroglial marker GFAP.

175 cords, along with reduction of the reactive astroglial marker GFAP.

176 This astroglial mechanism plays an important role in the auto

177 Here, we describe an astroglial mechanism that contributes to the protection

178 Astroglial mechanisms underlying this essential neuron-g

179 This study unravels H2 S as an astroglial mediator of motor neuron damage possibly invo

180 uroblast spatial boundaries within the dense astroglial meshwork of the SVZ and rostral migratory str

181 However, the role of astroglial metabolic networks in behavior is unclear.

182 Moreover, inhibition of astroglial metabolism (-35%, p < 0.01), vasoactive epoxy

183 which suppresses developmental expression of astroglial metabotropic glutamate receptor 5 (mGluR5), a

184 ecipitation and QRT-PCR analysis showed that astroglial mGluR5 (but not GLT1) mRNA is associated with

185 yphenylglycine-dependent Ca(2+) responses of astroglial mGluR5 receptor are also selectively reduced

186 (+) glutamatergic signaling, mediated by the astroglial mGluR5 receptor, regulates the functional mat

187 athway that selectively alters developmental astroglial mGluR5 signaling, unveiling astroglial molecu

188 gly and selectively diminishes developmental astroglial mGluR5 signaling.

189 provide in vivo evidence for AQP4-dependent astroglial migration and suggest that modulation of AQP4

190 Dysfunctional astroglial migration underlies the callosal dysgenesis i

191 Physiological decrease in PO2 inhibits astroglial mitochondrial respiration, leading to mitocho

192 AEDs) with fewer side effects by focusing on astroglial modulation of spatiotemporal seizure dynamics

193 ental astroglial mGluR5 signaling, unveiling astroglial molecular mechanisms involved in FXS pathogen

194 To determine the functional consequence of astroglial morphological plasticity on cued heroin seeki

195 lves respond to heroin cues or if changes in astroglial morphology are necessary for heroin seeking.

196 s of acute myelin breakdown, indicating that astroglial myelin phagocytosis is an early and prominent

197 slices, clamping [Ca(2+)]i at a low level in astroglial network resulted in an inhibition of NMDA EPS

198 nactivation of D-serine synthesis within the astroglial network resulted in the reduction of NMDA EPS

199 Here, we demonstrate that perturbation of astroglial networks impairs the sleep-wake cycle.

200 ct motor coordination, global suppression of astroglial networks may contribute to the cognitive effe

201 tes to neurons through gap junction-mediated astroglial networks.

202 Astroglial-neuronal interactions are important in brain

203 blocking antibody suggest that NaPB-induced astroglial neurotrophins are functionally active.

204 udy, we show that transgenic inactivation of astroglial NF-kappaB (glial fibrillary acidic protein-Ik

205 eceptor-mediated endocytosis and resulted in astroglial NF-kappaB activation and secretion of chemoki

206 rotein (APP) transgenic mice are worsened by astroglial NF-kappaB hyperactivation and resulting C3 el

207 h neuronal overproduction of Abeta activates astroglial NF-kappaB to elicit extracellular release of

208 Exposure to Abeta activates astroglial NFkappaB and C3 release, consistent with the

209 ereby Abeta acts as an upstream activator of astroglial nuclear factor kappa B (NF-kappaB), leading t

210 transplantation, consistent with a potential astroglial origin for mesenchymal GBM.

211 neuron specific), consistent with a possible astroglial origin.

212 tly rescues decreased mGluR5 function, while astroglial overexpression of miR-128-3p strongly and sel

213 eveals the fundamental physiological role of astroglial oxygen sensitivity; in low-oxygen conditions

214 ary acidic protein (GFAP) as a biomarker for astroglial pathology in neurological diseases provides b

215 Astroglial pathology is seen in various neurodegenerativ

216 describe novel astroglial pathway for synthesis of GABA, which is subse

217 The mechanisms underlying astroglial pH sensitivity remained unknown and here we s

218 month in the UVN-gabazine group whereas the astroglial population increased, and these animals showe

219 zone (VZ) of the injured tecta indicated an astroglial precursor response.

220 encephalic midline, FGF/ERK signaling drives astroglial precursor somal translocation from the ventri

221 esses the supply of translocation signals to astroglial precursors by a non-cell-autonomous mechanism

222 the transmission of translocation signals to astroglial precursors.

223 inity transporters expressed by perisynaptic astroglial processes (PAPs): this helps maintain point-t

224 downregulation of glutamate transporters on astroglial processes adjacent to accumbens synapses cont

225 and found that developmental arborization of astroglial processes and expression of functional protei

226 nd postsynaptic elements as well as adjacent astroglial processes and the perisynaptic extracellular

227 s expressed almost exclusively in peripheral astroglial processes in the adult rat brain.

228 antly decreases perisynaptic enshealthing of astroglial processes on synapses.

229 nt microdomain Ca(2+) transients in the fine astroglial processes that depended on the average rather

230 However, it is not known how astroglial processes themselves respond to heroin cues o

231 D1-MSN dendritic spines and synapse-proximal astroglial processes.

232 tively analyze developmental arborization of astroglial processes.

233 aturing blood vessels that are ensheathed by astroglial processes.

234 d tau in neuronal perikarya and perivascular astroglial processes.

235 d lowest in sleep and are most pronounced in astroglial processes.

236 These human astroglial progenitors and immature astrocytes will be u

237 Finally, the astroglial progenitors are either amplified for an exten

238 ualize and analyse radial progenitors, their astroglial progeny, and the microtubule cytoskeleton of

239 P(swe)/PS1(DeltaE9) mice was associated with astroglial proliferation and elevated expression of the

240 D2 antagonist eticlopride and did not cause astroglial proliferation or hypertrophy.

241 result of milder disease course and reduced astroglial proliferation was obtained by deletion of the

242 Astroglial proximity to accumbens synapses was estimated

243 in-induced motor abnormalities and decreased astroglial reaction and neuronal degeneration in brains

244 Astroglial reaction and subsequent monocyte recruitment

245 afferent terminals, trigger Ca(2+)-dependent astroglial release of ATP to modulate baroreflex sensiti

246 the last few decades, different pathways of astroglial release of neuroactive substances have been p

247 ese data reveal Cx43 hemichannels as a novel astroglial release pathway at play in basal conditions,

248 local DEX treatment significantly attenuated astroglial response and reduced neuronal loss in the vic

249 enon and reveal intrinsic limitations of the astroglial response to injury.

250 The triggers and timing of the different astroglial responses in acute lesions remain unclear.

251 MRI can distinguish distinct microglial and astroglial responses related to WMI progression and arre

252 renergic terminals, but has little effect on astroglial responsiveness to norepinephrine, suggesting

253 urification followed by RNA-Seq, we profiled astroglial ribosome-associated (presumably translating)

254 Astrocytes form an astroglial scar and produce chondroitin sulfate proteogl

255 represent a promising approach to attenuate astroglial scar and reduce neural loss around implanted

256 s, intermingled with astrocytes, facilitated astroglial scar border formation and sequestered invadin

257 te hypertrophy, and pronounced disruption of astroglial scar formation after SCI.

258 tivation and infiltration, whereas FBs alter astroglial scar formation and increase immune-cell infil

259 lar mechanisms, regulation, and functions of astroglial scar formation is fundamental to developing s

260 ced by molecular interventions that overcome astroglial scar or myelin-associated inhibitors are refr

261 nhibitory factors in degenerating myelin and astroglial scar prevent axonal growth in the adult brain

262 s (>10 microm), overlain by a dose-dependent astroglial scar-like formation and recruitment of phagoc

263 previously undescribed pattern of interface astroglial scarring at boundaries between brain parenchy

264 or a history of opiate use, did not have any astroglial scarring in the brain regions analysed.

265 l cases of acute blast exposure showed early astroglial scarring in the same brain regions.

266 with chronic blast exposure showed prominent astroglial scarring that involved the subpial glial plat

267 Astroglial scars surround damaged tissue after trauma, s

268 ure; however, the mechanisms of pathological astroglial secretion remain unclear.

269 st a role for polyphosphate as a mediator of astroglial signal transmission in the mammalian brain.

270 TD, p-LTD is independent of postsynaptic and astroglial signaling.

271 cular signature and functional properties of astroglial subtypes in the adult CNS remain largely unde

272 presence of mitogens, permits generation of astroglial subtypes over a long-term expansion (days 21-

273 d differentiation of hPSCs to astrocytes and astroglial subtypes remains elusive.

274 display phenotypic differences of different astroglial subtypes.

275 cultured hippocampal neurons by NaPB-treated astroglial supernatants and its abrogation by anti-TrkB

276 logical features of interactions between the astroglial swelling sensor transient receptor potential

277 stated sucrose seeking induced no changes in astroglial synaptic association.

278 er of synaptic connections was increased and astroglial synaptic coverage was reduced.

279 now show that presynaptic terminals regulate astroglial synaptic functions, GLT1/EAAT2, via kappa B-m

280 We identify complement protein C3 as an astroglial target of NFkappaB and show that C3 release a

281 Results demonstrate that astroglial tau pathology in CTE is composed of 4R-immuno

282 Moreover, mice with astroglial TDP-43 deletion develop motor, but not sensor

283 rocytes are largely unknown, and the role of astroglial TDP-43 loss to ALS pathobiology remains to be

284 ides (43)Gap26 and (37,43)Gap27), as well as astroglial toxin but not microglial inhibitors, given 3

285 Finally, intrathecal administration of an astroglial toxin, l-alpha-aminoadipate, reversed mechani

286 We found that the expression of astroglial translating mRNAs closely follows the dorsove

287 ibit a grossly enlarged IG due to precocious astroglial translocation and conditional Hs2st mutagenes

288 Rescue of the Hs2st (-/-) astroglial translocation phenotype by pharmacologically

289 al role of Hs2st is to suppress FGF-mediated astroglial translocation.

290 xpression and transcriptional dysfunction of astroglial transporter expression.

291 grate as neuronal chains within a network of astroglial tubes in the rostral migratory stream.

292 y remodel the morphology and organization of astroglial tubes to promote long distance, directional m

293 s occurs through the coordinated activity of astroglial vesicular monoamine transporter 2 (VMAT2) tog

294 ions and glutamate homeostasis, neuronal and astroglial volume changes, and ion exchange with vascula

295 sential subunit of VRAC and a key factor for astroglial volume homeostasis.

296 onstitute a molecular system that fine-tunes astroglial volume regulation by integrating osmosensing,

297 Genetic knock-out of the gene encoding the astroglial water channel aquaporin-4, which is important

298 rebrovascular pulsation, and is dependent on astroglial water channels that line paravascular CSF pat

299 ased to the extracellular space and that the astroglial water transport via AQP4 is involved in tau c

300 tral hippocampus and identify a role for the astroglial xCT in ventral dentate gyrus (vDG) in stress