ライフサイエンスコーパス: microglial cell

1 k genes and the phagocytic activity of mouse microglial cells.

2 and viral-induced inflammatory responses in microglial cells.

3 -induced Ca(2+) signalling and cell death in microglial cells.

4 d to control the expansion and activation of microglial cells.

5 factor (MIF), which results in a M2 shift of microglial cells.

6 ll surface and mediate reovirus infection of microglial cells.

7 cle from denervation prior to its effects on microglial cells.

8 y and facilitate GR nuclear translocation in microglial cells.

9 -induced neuroinflammatory responses in BV-2 microglial cells.

10 of monocytes/macrophages and resident brain microglial cells.

11 protective factors in the brain by monocytes/microglial cells.

12 ours and promoted infiltration of macrophage/microglial cells.

13 atory conditions in activated CD11b-positive microglial cells.

14 ized in significant amounts by astrocytes or microglial cells.

15 the brain rudiment, where they give rise to microglial cells.

16 aps, were cleared and taken up by cocultured microglial cells.

17 n are also observed in both murine and human microglial cells.

18 ry bulb hosts a large population of resident microglial cells.

19 eta at Ser-8 also decreases its clearance by microglial cells.

20 fractalkine) which controls key functions of microglial cells.

21 ) was strongly upregulated by pilocarpine in microglial cells.

22 a major Abeta-degrading enzyme released from microglial cells.

23 as pain-related proteins and ion channels in microglial cells.

24 alic acid-binding receptor on the surface of microglial cells.

25 ts in the DKO eyes and LPS activated culture microglial cells.

26 ion of IDE leads to elevated MIP-1 levels in microglial cells.

27 represented a degenerating subpopulation of microglial cells.

28 p21(ras) and NF-kappaB in MPP(+)-stimulated microglial cells.

29 d nuclear factor-kappaB (NF-kappaB) in mouse microglial cells.

30 he blood-brain-barrier and reach neurons and microglial cells.

31 ecretion of tumor necrosis factor-alpha from microglial cells.

32 ired the clearance of extracellular Abeta by microglial cells.

33 or protein TIRAP and TLR2 in macrophages and microglial cells.

34 lid S8 and B8 did not impact inflammation in microglial cells.

35 occurred preferentially in glioma cells over microglial cells.

36 the secretion of inflammatory cytokines from microglial cells.

37 mice to Mn(2+) had similar effects in brain microglial cells.

38 asal respiratory rate, and spare capacity in microglial cells.

39 roliferation and triggering the formation of microglial cells.

40 yte precursor cells through a crosstalk with microglial cells.

41 ults show that the proliferation of resident microglial cells accounts for the expansion of the popul

42 In cultured primary rat microglial cells activated by lipopolysaccharide, safina

43 The source of CatS activity is microglial cells activated by the peripheral nerve injur

44 Changes in microglial cell activation and distribution are associat

45 ovel role for autophagy in the regulation of microglial cell activation and pro-inflammatory molecule

46 otential roles for Runx1 in the processes of microglial cell activation and proliferation and in neur

47 ophy, retinal photoreceptor dysfunction, and microglial cell activation in the affected areas.

48 In particular, microglial cell activation is believed to be associated

49 potent neuroprotective effects by inhibiting microglial cell activation through a beta2AR/beta-arrest

50 Microglial cell activation was concomitant with increase

51 se models of Alzheimer's disease by altering microglial cell activation.

52 Excessive microglial cells activation in response to inflammatory

53 neonates and infants, approaches to regulate microglial cell activity are likely to be important.

54 PGRN is most strongly expressed by activated microglial cells after injury.

55 IGF-1 in a subset of activated/proliferating microglial cells after stroke.

56 deletion of Irf8 in retinal cells, including microglial cells and a third mouse strain with targeted

57 n stem, cortex and thalamus by CD68 positive microglial cells and activation of astrocytes.

58 lity of the TSPO ligands to detect activated microglial cells and astrocytes.

59 ng USP33 and downstream ATF3 levels in human microglial cells and contributes in neuroinflammation wi

60 st that long-term interaction occurs between microglial cells and deafferented cochlear nucleus neuro

61 3 expression reduced the number of activated microglial cells and decreased apoptosis of neuronal cel

62 uropathogenesis of HIV-1 using primary human microglial cells and determined whether opiates converge

63 lose and rapamycin activate autophagy in BV2 microglial cells and down-regulate the production of pro

64 CD11b(+) infiltrating monocytes and resident microglial cells and down-regulates the expression of MH

65 nduce that activation of the inflammasome in microglial cells and give rise to IL-1beta release, whic

66 ion of miR-301a is increased in JEV-infected microglial cells and human brain.

67 domain containing 3 (NLRP3) inflammasomes in microglial cells and in HIV-Tg rats administered lipopol

68 The activation of microglial cells and infiltration of Th1 cells resulted

69 ere affected as well, primarily in activated microglial cells and macrophages.

70 emphasized the pathogenic contributions from microglial cells and motivated studies of microglial fun

71 with cerebral endothelial cells to activate microglial cells and promote sickness behavior.

72 n (GFAP) was performed to identify activated microglial cells and reactive astrocytes.

73 rsolic acid also blocked binding of Abeta to microglial cells and subsequent ROS production.

74 neuronal IFNbeta, which, in turn, activates microglial cells and subsequently manifests the infiltra

75 production of pro-inflammatory molecules in microglial cells and their effects on neuronal cells.

76 to elucidate the fine structural features of microglial cells and their processes in the hilar region

77 to describe the ultrastructural features of microglial cells and their processes.

78 (NK) cells, NK-T cells, gammadelta T cells, microglial cells, and astrocytes.

79 aenoyl ethanolamide (EPEA) by activated BV-2 microglial cells, and by human CYP2J2.

80 netration, Abeta capture and degradation via microglial cells, and cholinergic dysfunction ameliorati

81 elated antimicrobial peptide in macrophages, microglial cells, and dendritic cells.

82 cerebellar Purkinje cells, oligodendrocytes, microglial cells, and dopaminergic neurons was not signi

83 Caspase-4 was expressed predominantly in microglial cells, and in the presence of CASP4, more mic

84 These EVs get internalized by human microglial cells, and miR-148a suppresses the ubiquitin-

85 eration and differentiation into astrocytes, microglial cells, and neurons were revealed using immuno

86 d numbers of activated T cells, macrophages, microglial cells, and neutrophils in the affected brain

87 ycline, which affects monocytes/macrophages, microglial cells, and PMNs, had significantly fewer seiz

88 Microglial cells are a specialized population of macroph

89 During diabetes, retinal microglial cells are activated to release inflammatory c

90 P2Y1/P2Y13 receptors.SIGNIFICANCE STATEMENT Microglial cells are brain-resident immune cells with mu

91 Microglial cells are considered as sensors of brain path

92 Microglial cells are difficult to track during developme

93 ndicating monocytes/macrophages and resident microglial cells are important in seizure development.

94 ED-1 positive microglial cells are observed accompanying the entire co

95 Microglial cells are phagocytes in the central nervous s

96 Microglial cells are professional phagocytes of the CNS

97 After cell damage, microglial cells are rapidly activated, initiating a ser

98 in health and disease.SIGNIFICANCE STATEMENT Microglial cells are resident macrophages of the CNS, wi

99 ies provide evidence that ONH astrocytes and microglial cells are the primary sources for the TNF-alp

100 Microglial cells are the resident macrophages of the cen

101 Microglial cells are the resident tissue macrophages of

102 neuropathologic demonstration that activated microglial cells are the source of diffuse NAWM inflamma

103 mechanism and identifies IGFBP1 released by microglial cells as a novel mediator of MCSF-induced ang

104 omitantly decreased the numbers of activated microglial cells as determined by MHCII expression.

105 ranulocytes (neutrophils), Muller cells, and microglial cells as TNF-alpha sources.

106 Quinolinic acid was produced by microglial cells, as expression of the quinolinic acid-p

107 ove that inflammatory cytokine production by microglial cells, astrocytes, neutrophils, and monocytes

108 onsistent decrease (a) in the recruitment of microglial cells at the lesioned site and (b) in the pro

109 small side branch arise within 5 mum of the microglial cell body.

110 In vitro, both endothelial and microglial cells bound and internalized PGPFs before tra

111 In this context, extension of microglial cell branches toward cell debris underlies th

112 ippocampus via cell-cell contacts, mediating microglial cell branching in the presence of inflammatio

113 Microglial cells but not infiltrating leukocytes or othe

114 nal cells showed poor survival and attracted microglial cells, but CSPG was not greatly induced.

115 probe, for analyzing the metabolome of live microglial cells by drift-tube ion mobility spectrometry

116 any morphological and functional states that microglial cells can adopt.

117 the deubiquitination machinery of the human microglial cell (CHME3).

118 Microglial cells comprising the brain's immune system ar

119 00 years, yet recent data have revealed that microglial cells constitute a sizeable proportion of ven

120 Microglial cells constitute the resident immune cell pop

121 We found that microglial cells constitute ~7% of non-neuronal cells in

122 verity and volume of injury, suggesting that microglial cells contribute to endogenous protection dur

123 reciprocal interactions between neurons and microglial cells control the functional maturation of co

124 Microglial cell counts were obtained from retinal wholem

125 ation and prion infectivity in primary sheep microglial cell cultures (PRNP 136VV/154RR/171QQ) and Ro

126 inhibited uptake and clearance of Abeta42 in microglial cell cultures.

127 ne protein release in primary astroglial and microglial cell cultures.

128 ake and clearance of amyloid beta (Abeta) in microglial cell cultures.

129 sease, a targeted overexpression of IL-10 in microglial cells, delivered via viral vectors expressed

130 To test this hypothesis, we determined microglial cell densities (the inverse of cell size) usi

131 was significantly associated with increased microglial cell density.

132 were effectively applied to FACS analysis of microglial cells derived from a mouse model relevant to

133 implicated in ALS pathology, we used primary microglial cells derived from transgenic SOD1-G93A mice

134 gnal mapped closely to the area of activated microglial cells detected by immunohistochemistry.

135 f CD11b and Iba1, commonly used for labeling microglial cells, did not differ in the three patient gr

136 Furthermore, activation of microglial cells, DNA fragmentation, and apoptosis of in

137 Numbers of astrocytes and microglial cells do not appear to increase with age, but

138 RV-W ENV induces a degenerative phenotype in microglial cells, driving them toward a close spatial as

139 We propose that immune activation of microglial cells during development, superimposed upon g

140 In cultured microglial cells, EP4 stimulation attenuated levels of A

141 Minigene RNA splicing studies in BV2 microglial cells established that rs12459419 is a functi

142 oncomitant with morphological alterations in microglial cells, even though a significant increase in

143 To determine whether microglial cells exert injurious effects after neonatal

144 n, the stimulation of CB2R, overexpressed in microglial cells, exerts beneficial effects in neurodege

145 Furthermore, primed microglial cells exposed to exosomes from Mn-treated mic

146 Both ONH astrocytes and microglial cells expressed delta-, kappa-, and mu-opioid

147 ith complement proteins may be eliminated by microglial cells expressing complement receptors.

148 The area of CD11b-expressing microglial cells extended beyond that of enhanced GFAP s

149 ysosomal accumulation of heparan sulphate in microglial cells followed by their activation and cytoki

150 howed that NLRP3 was up-regulated in retinal microglial cells following pONC, propagating from the in

151 ssion of sialic acid, are required in murine microglial cells for efficient reovirus binding and infe

152 lead to new strategies to selectively target microglial cells for oncolytic applications.

153 gical reactivity and an increased density of microglial cells from 2 to 20 days after injury.

154 t resulted in the phenotypic polarization of microglial cells from a proinflammatory M1 state, into a

155 CD33 is upregulated on microglial cells from post-mortem AD patient brains, and

156 In microvessels, motor neurons, and microglial cells from SOD1-mutant mice and in cultured n

157 ther represented an accumulation of resident microglial cells from within the retina.

158 Microglial cell function is implicated in the etiology o

159 In stimulated microglial cells, H2BK20ac was more correlated with cell

160 Recently, microglial cells have been shown to be responsible for a

161 ing CCI, ultrastructural studies reveal that microglial cells have very irregular shapes and have man

162 both induced and basal HIV transcription in microglial cells (HC69) and monocytic cell lines (U1 and

163 und inhibits LPS-induced TNFalpha release in microglial cells, HIV-1 Tat-induced release of cytokines

164 Proteomics analyses of exosomes of cultured microglial cells identified a large number of proteins,

165 hanges in the distribution and morphology of microglial cells (immunostained with the ionized calcium

166 our data indicated that caspase-4 modulates microglial cells in a manner that increases proinflammat

167 Studying microglial cells in acute brain slices, we found that TL

168 we observed increased expression of CD33 in microglial cells in AD brain.

169 cortex indicated a potential involvement of microglial cells in contributing to the structural and f

170 studied how pentobarbital affects BV2 mouse microglial cells in culture.

171 trophic lateral sclerosis (ALS), the role of microglial cells in events initiating and/or precipitati

172 nic receptor neuropilin 1 in macrophages and microglial cells in gliomas as a pivotal modifier of tum

173 RIPK1 is highly expressed by microglial cells in human AD brains.

174 is study we found increased proliferation of microglial cells in human Alzheimer's disease, in line w

175 autophagy and HIV-1 pathogenesis mediated by microglial cells in opioid-abusing individuals.

176 n assay to study the phenotypic behaviour of microglial cells in primary neuronal co-cultures through

177 o inactivation of type I NKT cells, DCs, and microglial cells in suppression of autoimmunity.

178 a chronic inflammatory reaction mediated by microglial cells in the brain is particularly strong in

179 Microglial cells in the brain tumor microenvironment are

180 n channel that is predominantly expressed on microglial cells in the central nervous system.

181 s-sectional area and Iba-1 immunostaining of microglial cells in the cochlear nucleus was observed at

182 We investigated the function of microglial cells in the developing cerebral cortex of pr

183 tory cytokine tumor necrosis factor-alpha by microglial cells in the familial AD APP(swe)/PS1(DeltaE9

184 ed by the presence of reactive and senescent microglial cells in the frontal cortex.

185 mutant mice generated a large population of microglial cells in the olfactory bulb and reduced the d

186 BV-2 mouse microglial cells in the presence and absence of pentobar

187 Far fewer invasive macrophage/microglial cells in the subretinal space and weaker acti

188 ne marrow chimera experiments confirmed that microglial cells in the subretinal space were not recrui

189 murine BV-2 cells and both sex primary mouse microglial cells, in a dose- and time-dependent fashion.

190 The role of resident brain macrophages-microglial cells-in stroke remains controversial.

191 f CEMIP(+) exosomes by brain endothelial and microglial cells induced endothelial cell branching and

192 Accumulative evidence indicates that microglial cells influence the normal development of bra

193 A microglial cell is both a glial cell of the central nerv

194 The proliferation and activation of microglial cells is a hallmark of several neurodegenerat

195 tions or rare variants in genes expressed in microglial cells, known to regulate immune functions, or

196 To understand whether microglial cells limit injury after neonatal stroke by p

197 chemokines and cytokines produced by a mouse microglial cell line (BV-2 cells).

198 tured primary retinal microglia and a murine microglial cell line (BV-2), we found that these cells e

199 ncrease intracellular GSH levels in a murine microglial cell line (BV2), of which dimercaprol (2,3-di

200 ivity and uptake of Staphylococcus aureus in microglial cell line BV-2 in a kinase-dependent manner.

201 increase in LPS-treated immortalized murine microglial cell line BV2 cells in an MPTP-induced mouse

202 rons and microglia, as well as by the murine microglial cell line BV2, and it was induced by inflamma

203 sis of blood neutrophils and monocytes and a microglial cell line revealed that unlike CD33M, the CD3

204 ical modeling, using TNFalpha to stimulate a microglial cell line stably overexpressing Hsp72.

205 ne response of primary human monocytes and a microglial cell line to pathologic forms of alpha-synucl

206 with this hypothesis, in vitro culture of a microglial cell line with Interferon-beta, but not infec

207 sion induced by EP2 receptor activation in a microglial cell line, reinforcing the use of EP2 antagon

208 d in primary microglial cultures and the BV2 microglial cell line.

209 led an investigation of endogenous P2X4 in a microglial cell line.

210 , and expression of a mutant htt fragment in microglial cell lines was sufficient to reproduce these

211 es ASPP2 expression in murine macrophage and microglial cell lines, a human monocyte cell line, and p

212 tPA(-/-)) mice and in mice that lack LRP1 in microglial cells (macLRP(-)).

213 Although immune activation of microglial cells may over time engage various signal tra

214 (CXCR4) on invading tumor cells, macrophage/microglial cells (MGCs), and glioma stem cells (GSCs).

215 In the present study, we analyzed whether microglial cells might sense CSD by recording membrane c

216 on of c-Fos and activation of astrocytes and microglial cells, NR1 and NR2B receptors, Src within the

217 brain and exist in the absence of changes in microglial cell number, but with putative evidence of mi

218 Flow cytometric analysis of microglial cells obtained from infected brain tissue dem

219 We find that microglial cells occur in similar densities in the brain

220 n colonic macrophages and spinal neurons and microglial cells of mice with colitis.

221 Silencing IGFBP1 expression in microglial cells or its neutralization by an antibody re

222 TSPO expression was associated with microglial cells or macrophages without obvious astrocyt

223 We discovered that in presymptomatic disease microglial cells overexpress anti-inflammatory cytokine

224 high neuronal densities and therefore fewer microglial cells per neuron.

225 e adult neurogenesis, showing that activated microglial cells per se, and not the lack of sensory exp

226 Thus, microglial cells play a previously unrecognized protecti

227 Microglial cells play essential volume-related actions i

228 Microglial cell-polarization correlated with maximal exp

229 ronal TNF-RII may act nonautonomously on the microglial cell population.

230 One day after sensory deafferentation, microglial cells proliferate in the olfactory bulb, and

231 GW2580, a selective CSF1R inhibitor, reduced microglial cell proliferation in SOD1(G93A) mice, indica

232 We found that microglial cell proliferation in the spinal cord of SOD1

233 wn about the mechanisms controlling amoeboid microglial cell proliferation, activation, and ramificat

234 Cumulatively, in two species, we show that microglial cells protect neonatal brain from hemorrhage

235 ng neurons, lessened the number of activated microglial cells, protected cerebral blood flow (CBF), a

236 jected postnatal day 7 (P7) rats depleted of microglial cells, rats with inhibited microglial TGFbr2/

237 hin the barrels and CX3CR1 deficiency delays microglial cell recruitment into the barrel centers.

238 splayed accumulation of GC and GS, activated microglial cells, reduced number of neurons and aberrant

239 ich is expressed by neurons, astrocytes, and microglial cells, regulates inflammatory and repair proc

240 ng in turn that the volume monitored by each microglial cell remains constant across mammals.

241 that Bregs modulate T lymphocyte as well as microglial cell responses within the infected brain and

242 As a consequence, we find that one microglial cell services as few as one and as many as 10

243 perikarya, and in the case of astrocytes and microglial cells some of these inclusions are phagocytos

244 can be targeted therapeutically to modulate microglial cell state and slow the progression of AD.

245 BV-2 microglial cells stimulated with low doses of interferon

246 and CD80 on infiltrating macrophages and on microglial cells suggested a role for T cell and Ag-pres

247 p21(ras) and p21(rac) activation by NaPB in microglial cells suggests that NaPB exerts anti-inflamma

248 In contrast, microglial cells support young neurons.

249 markedly increased this inhibitory effect on microglial cells, supporting a causal link to disease et

250 voring retention of this glycoprotein on the microglial cell surface and augmenting its phosphatase a

251 Rare sequence variants in the microglial cell surface receptor TREM2 have been shown t

252 partner Mrp8 was found to be upregulated in microglial cells surrounding amyloid plaques.

253 This work elucidates host genes that render microglial cells susceptible to reovirus infection and e

254 s demonstrated significantly fewer activated microglial cells than control groups.

255 r MMP-1, -3, and -9 gene expression in human microglial cells than direct infection.

256 in naloxone-treated DKO animals and cultured microglial cells than in controls, as were serum nitrite

257 y bulb SQSTM1 often congregated in activated microglial cells that also contained olfactory marker pr

258 ds current understanding of the receptors on microglial cells that are engaged by reovirus.

259 In these mice, we identified activated microglial cells that likely were recruited to transport

260 findings about the steady-state functions of microglial cells, the factors that are important for phy

261 Up-regulation of CB2R on activated microglial cells, the first step in neurodegeneration, h

262 re endocytosed through caveolae into primary microglial cells, thereby mounting neuroinflammatory res

263 sp70 induced IFN-beta transcription in mouse microglial cells through Toll-like receptors 2 and 4.

264 x1 expression in activated and proliferating microglial cells throughout the neurogenic regions.

265 In vitro, addition of activated BV2 microglial cells to hippocampal cultures increased neuro

266 d activation and polarization of the primary microglial cells to inflammatory M1 phenotype with the s

267 tor complex, Toll-like receptor 4 (TLR4), on microglial cells to initiate central innate immune signa

268 We thus conclude that the addition of microglial cells to mammalian brains is governed by mech

269 Exposing activated mouse microglial cells to Mn(2+) substantially augmented NLRP3

270 ti-ferritin, we have studied the response of microglial cells to neonatal CNS infection with PVC-211

271 Furthermore, TNF-alpha recruited microglial cells to provide sIL-6R, which can form compl

272 peripheral noxious stimulation and recruits microglial cells to provide soluble IL-6 receptor, which

273 hine at 100 nm enhanced migration of primary microglial cells toward adenosine diphosphate by 257, 24

274 in DR, we performed additional studies using microglial cells treated with Amadori-glycated albumin,

275 s elicited by the supernatant from monocytes/microglial cells treated with conditioned medium from gl

276 ced the ability of supernatants derived from microglial cells treated with glioma cell-conditioned me

277 xpression of mir-146a in primary human fetal microglial cells upon infection with HIV-1 and found inc

278 the liver, Kupffer cells, and in the brain, microglial cells use alpha(X)beta(2) to control fungal i

279 Generation of a P2X7-deficient clone of BV-2 microglial cells using CRISPR/Cas9 gene editing enabled

280 n streptozocin-injected rats and in isolated microglial cells using immunofluorescence, enzyme-linked

281 Data demonstrate that mouse microglial cells via CR3 recognize and remove neuronal s

282 The deficiency in viral replication in microglial cells was associated with silencing of partic

283 However, the presence of activated microglial cells was not correlated directly with the pr

284 s differentiate during development to create microglial cells, we investigated CX3CR1 and CCR2 transc

285 aging the morphology of dendritic spines and microglial cells well below the surface of acute brain s

286 y cytokines (Arg1, Nos2, Tnf) in LPS treated microglial cells were assessed using solubilised and sol

287 Additionally, microglial cells were frequently seen apposing the cell

288 Migratory Iba1+ microglial cells were localized to the RPE apical surfac

289 f monocytes and platelets, and activation of microglial cells were measured by flow cytometry.

290 delta(-/-) mice was reduced and the resident microglial cells were not activated.

291 an optic nerve head (ONH) astrocytes and rat microglial cells were treated with morphine (0.1-1 muM)

292 ctoderm; 2) at E10.5, CX3CR1 single-positive microglial cells were visualized penetrating the neuroep

293 Here we show that microglial cells, which are viewed as pathologic sensors

294 Fcgamma receptor-mediated overactivation of microglial cells, which may contribute to an inappropria

295 Here we report on a distinct subset of microglial cells, which we term periventricular microgli

296 mmatory cytokines and an M1 phenotype in the microglial cells while downregulating anti-inflammation

297 ine release after LPS stimulation in primary microglial cells, while it did not affect the viability

298 or molecule 1; Iba-1) and the interaction of microglial cells with deafferented neurons in the ventra

299 This was associated in cultured murine microglial cells with decreased Akt and I-kappaB kinase

300 icroglia, and treatment of Rag-5xfAD mice or microglial cells with preimmune IgG enhances Abeta clear