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 fibrillary acidic protein (GFAP) represents astroglial activation and gliosis during neurodegenerati

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

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

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

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 ess direct growth effects absent vascular or astroglial activity.

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

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

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

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

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

15 Astroglial and microglial activation, reduced neuronal d

16 hypersensitivity caused by augmented spinal astroglial and microglial activity.

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

18 S immunoreactivity was expressed within both astroglial and microglial cells and there was marked cel

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

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

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

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

23 LGN is expressed in neuronal, astroglial, and microglial cultures, whereas AGS3 expres

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

25 f-renewal and differentiation into neuronal, astroglial, and oligodendroglial phenotypes.

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

27 egy with modification of inhibitory reactive astroglial-associated extracellular matrix could enhance

28 ical interaction between regrowing axons and astroglial-associated fibronectin in white matter may be

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

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

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

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

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

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

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

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

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

38 growth and survival advantage as well as the astroglial cell differentiation defect were completely r

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

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

41 nel in the brain, expressed predominantly in astroglial cell membranes.

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

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

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

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

46 Astroglial cells also express AMPA receptors, but their

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

48 rter-1 (GLT-1) is expressed predominantly in astroglial cells and is responsible for the largest prop

49 of glial fibrillary acidic protein positive astroglial cells and MAC-1 ir microglia.

50 nitric-oxide synthase (iNOS) in human U373MG astroglial cells and primary astroglia.

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

52 fen) injections induced Cre recombination in astroglial cells at postnatal day 5 and allowed us to pe

53 In addition, many astroglial cells became more branched and stellate in mo

54 To identify the fates that astroglial cells can attain in the postnatal brain, we g

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

56 ults indicate an essential role for reactive astroglial cells in preventing neural graft integration

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

58 Muller cells in retina, which are similar to astroglial cells in the central nervous system, where AQ

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

60 umbers of morphologically abnormal, immature astroglial cells in vitro.

61 ot that of the CAT gene as RSV-CAT in U373MG astroglial cells led to the induction of NO production a

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

63 by gemfibrozil in cytokine-stimulated U373MG astroglial cells suggests that this compound inhibits th

64 ased astrocyte proliferation that may render astroglial cells susceptible to neoplastic transformatio

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

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

67 nation, reporter-tagged cells were quiescent astroglial cells that expressed the stem cell marker LeX

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

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

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

71 ts but is also detected in a subset of GFAP+ astroglial cells, ependymal cells, and Dlx2+ precursors

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

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

74 Similar to U373MG astroglial cells, RSV-tat also induced the production of

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

76 B is a calcium-binding protein, localized to astroglial cells, which has a variety of neurotrophic fu

77 of FMRP in regulating protein expression in astroglial cells.

78 greater sensitivity to thiopurine therapy in astroglial cells.

79 n the extensive activation of microglial and astroglial cells.

80 lutamate transporters primarily expressed in astroglial cells.

81 found in areas enriched with microglial and astroglial cells.

82 0B is a calcium-binding protein found within astroglial cells.

83 a but not that of GAS in cytokine-stimulated astroglial cells.

84 e opioid mu receptor that we demonstrated on astroglial cells.

85 tive expression of the opioid mu receptor on astroglial cells.

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

87 rminants of transport activity in individual astroglial cells.

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

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

90 gradation of Abeta and implicate deficits in astroglial clearance of Abeta in the pathogenesis of AD.

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

92 Astroglial CNTF expression was not affected by diffusibl

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

94 In the presence of C6 astroglial co-culture b.End3 monolayers achieved a maxim

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

96 Primary astroglial cultures from cKO mice expressed elevated fib

97 e and l-[(14)C]lactate to (14)CO(2), whereas astroglial cultures oxidized both substrates sparingly a

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

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

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

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

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

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

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

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

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

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

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

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

110 the radial glial scaffolding with premature astroglial differentiation, and 2) thickening of the mar

111 erentiation was accompanied by inhibition of astroglial differentiation.

112 esults in DNA hypomethylation and precocious astroglial differentiation.

113 sms that control the timing and magnitude of astroglial differentiation.

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

115 The astroglial distribution of the two glutamate transporter

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

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

118 Astroglial dysfunction is known to be present in HE.

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

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

121 To study astroglial energy metabolism and the directionality of l

122 rized by unmyelinated axons and perisynaptic astroglial envelopes.

123 e animals mediates the stimulatory effect of astroglial erbB receptor activation on neuronal LHRH rel

124 Hypothalamic astroglial erbB tyrosine kinase receptors are required f

125 ATP transmits astroglial excitation to the brainstem respiratory netwo

126 To assess the significance of astroglial export of lactate to neurons in vivo, we atte

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

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

129 .End3 cells were grown in the presence of C6 astroglial factors.

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

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

132 ic protein demonstrated that SHG arises from astroglial filaments.

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

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

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

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

137 ivo modulation of FXS synaptic phenotypes by astroglial FMRP.

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

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

140 for melatonin receptors in the regulation of astroglial function, impacting specific brain regions di

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

142 olecular atlas for exploring region-specific astroglial functions.

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

144 9 transcription, suggesting that TNF induces astroglial Gal-9 through the TNF/TNFR1/JNK/cJun signalin

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

146 nct nonoverlapping cell populations, whereas astroglial GFAP appeared, in the absence of other neural

147 In contrast, astroglial glial fibrillary acidic protein (GFAP) was no

148 oduct of Glu metabolism, is synthesized from astroglial Gln and contributes to total Glu/Gln neurotra

149 Blockade of astroglial glutamate reuptake potentiated NSV-induced mo

150 Astroglial glutamate transport was reduced markedly in t

151 8:A > C (g.-181A > C) SNP in the promoter of astroglial glutamate transporter (EAAT2) and the same ap

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

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

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

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

156 We found that astroglial glutamate transporter subtype glutamate trans

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

158 Altered expression of astroglial glutamate transporters accompanied by reduced

159 transporter knock-out mice revealed that the astroglial glutamate transporters GLT-1 and GLAST, but n

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

161 particularly via expression and function of astroglial glutamate transporters.

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

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

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

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

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

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

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

169 players is associated with acute axonal and astroglial injury.

170 oordinate the facilitatory transsynaptic and astroglial input to LHRH neurons during sexual developme

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

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

173 acetate (50 mgkg) intravenously to stimulate astroglial lactate oxidation and then examined the effec

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

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

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

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

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

179 Moreover, when astroglial lipid synthesis was inhibited, oligodendrocyt

180 ndent glutamate transporter with predominant astroglial localization.

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

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

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

184 c neuropil territories to form a stereotyped astroglial map.

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

186 ic period, DNA methylation inhibits not only astroglial marker genes but also genes that are essentia

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

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

189 s within and outside the VZ also express the astroglial marker glutamine synthetase (Glns).

190 Astroglial mechanisms underlying this essential neuron-g

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

192 This astroglial-meningeal fibroblast scar is fully developed

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

194 were fitted with a two-compartment neuronal-astroglial metabolic model.

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

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

197 Concomitant activation of astroglial metabotropic and AMPA receptors results in th

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

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

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

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

202 Dysfunctional astroglial migration underlies the callosal dysgenesis i

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

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

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

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

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

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

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

210 Astroglial-neuronal interactions are important in brain

211 However, its role in modulating astroglial-neuronal relationships is poorly understood.

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

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

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

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

216 e demonstrate that selective inactivation of astroglial NF-kappaB in transgenic mice expressing a dom

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

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

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

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

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

222 usceptibility to excitotoxic injury, whereas astroglial overexpression of TGF-beta1 protects adult mi

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

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

225 Astroglial pathology is seen in various neurodegenerativ

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

227 fibrillary acidic protein (GFAP; a marker of astroglial phenotype).

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

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

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

231 antly decreases perisynaptic enshealthing of astroglial processes on synapses.

232 tively analyze developmental arborization of astroglial processes.

233 aturing blood vessels that are ensheathed by astroglial processes.

234 creased glutamate synapses and retraction of astroglial processes.

235 These human astroglial progenitors and immature astrocytes will be u

236 Finally, the increase in astroglial progenitors and proliferating cells seen in v

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

238 + progenitor cells, suggesting that immature astroglial progenitors may serve as a reservoir of proli

239 bited expression of proteins associated with astroglial progenitors, including nestin and brain lipid

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

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

242 ET-1 induces astroglial proliferation in cultured human optic nerve h

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

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

245 ounced in areas of the MTLE hippocampus with astroglial proliferation, even though astrocytes normall

246 T2; refs 1, 2), the physiologically dominant astroglial protein.

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

248 Astroglial reaction and subsequent monocyte recruitment

249 k), suggesting that the Erk pathway controls astroglial regulation of apoE expression in neuronal cel

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

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

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

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

254 onal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific mar

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

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

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

258 Astrocytes form an astroglial scar and produce chondroitin sulfate proteogl

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

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

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

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

263 uronal cell death and lesion volume, reduced astroglial scar formation and microglial activation, and

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

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

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

267 ate filaments in astrocytes and formation of astroglial scar tissue.

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

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

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

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

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

273 Astroglial scars surround damaged tissue after trauma, s

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

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

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

277 In contrast, astroglial Sp-factors activated promoter activity throug

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

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

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

281 display phenotypic differences of different astroglial subtypes.

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

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

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

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

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

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

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

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

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

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

295 The astroglial water channel aquaporin-4 (AQP4) facilitates

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

297 aster in mice lacking aquaporin-4 (AQP4), an astroglial water channel that facilitates fluid movement

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