ライフサイエンスコーパス: microglial cell

1 e fluorescent chromophore is retained by the microglial cell.

2 roliferation and triggering the formation of microglial cells.

3 atory conditions in activated CD11b-positive microglial cells.

4 ized in significant amounts by astrocytes or microglial cells.

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

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

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

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

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

10 fractalkine) which controls key functions of microglial cells.

11 ) was strongly upregulated by pilocarpine in microglial cells.

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

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

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

15 yte precursor cells through a crosstalk with microglial cells.

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

17 represented a degenerating subpopulation of microglial cells.

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

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

20 effects may be mediated by direct action on microglial cells.

21 euronal injury induces IL-1beta release from microglial cells.

22 )ARs are abundantly expressed in rat retinal microglial cells.

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

24 nd CD68) in mouse primary microglia and BV-2 microglial cells.

25 and viral-induced inflammatory responses in microglial cells.

26 was detected in astrocytes and in macrophage-microglial cells.

27 ay for paraquat-induced cytotoxicity to BV-2 microglial cells.

28 in human and murine alveolar macrophages and microglial cells.

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

30 iously undescribed MGL activity expressed by microglial cells.

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

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

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

34 y and facilitate GR nuclear translocation in microglial cells.

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

36 of monocytes/macrophages and resident brain microglial cells.

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

38 ours and promoted infiltration of macrophage/microglial cells.

39 olling autoimmune inflammation by inducing a microglial cell aaMphi phenotype.

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

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

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

43 Changes in microglial cell activation and distribution are associat

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

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

46 strated that IFN-gamma was critical for both microglial cell activation and the anticryptococcal effi

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 (+) T cells were not required for either the microglial cell activation or anticryptococcal efficacy

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

51 Microglial cell activation was concomitant with increase

52 y, while peripheral IFN-gamma production and microglial cell activation were observed early after tre

53 Excessive microglial cells activation in response to inflammatory

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

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

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

57 ), an upstream regulator of PGE2 release, to microglial cells and a neuronal localization of the PGE2

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

59 CD68 positive microglial cells and activated GFAP positive astrocytes

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

61 Activated microglial cells and astrocytes were present in thalamus

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

63 glycoprotein amino acids 35-55 (MOG(35-55)), microglial cells and CNS-infiltrating myeloid dendritic

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

65 3 expression reduced the number of activated microglial cells and decreased apoptosis of neuronal cel

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

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

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

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

70 oglia, we have developed a method to isolate microglial cells and infiltrating leukocytes from adult

71 tor-activated receptor-alpha (PPAR-alpha) in microglial cells and isolating primary microglia from PP

72 Iba1 is a marker for microglial cells and previous immunocytochemical studies

73 and proinflammatory cytokines in mouse BV-2 microglial cells and primary microglia.

74 was a marked increase in both the number of microglial cells and processes per cell visualized in vi

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

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

77 Activation of cultured microglial cells and subsequent release of nitric oxide

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

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

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

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

82 e in mediating paraquat cytotoxicity in BV-2 microglial cells and this process is mediated through PK

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

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

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

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

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

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

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

90 Microglial cells are a specialized population of macroph

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

92 Microglial cells are difficult to track during developme

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

94 The results suggest that microglial cells are necessary for the usual sprouting o

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

96 Microglial cells are phagocytes in the central nervous s

97 Microglial cells are professional phagocytes of the CNS

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

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 r cell death, recent studies have implicated microglial cells as a major producer of ROS for damaging

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

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

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

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

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

109 to demonstrate the morphological features of microglial cells at the light microscopic level.

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

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

112 Microglial cells but not infiltrating leukocytes or othe

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

114 Based on reports that activated murine microglial cells, but not human microglial cells, expres

115 ocyte-derived macrophages and brain-resident microglial cells by viral proteins as well as by the pro

116 Activated microglial cells can cause oligodendrocyte damage and wh

117 Microglial cells comprising the brain's immune system ar

118 Microglial cells constitute the resident immune cell pop

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

120 reactive oxygen species (ROS) and activated microglial cells contribute to neuronal loss, nuclear fa

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

122 Total microglial cell counts were made by using Iba-1 antibody

123 Microglial cell counts were obtained from retinal wholem

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

125 Sheep microglial cell cultures, derived from a prnp 136VV/171Q

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

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

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

129 Following exposure to PrP(Sc), sheep microglial cells demonstrated relatively low levels (tra

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

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

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

133 In addition to immortalized microglial cells, dieldrin induced a concentration-depen

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

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

136 lex virus (HSV)-1 brain infection stimulates microglial cell-driven proinflammatory chemokine product

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

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

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

140 To determine whether microglial cells exert injurious effects after neonatal

141 vated murine microglial cells, but not human microglial cells, express inducible nitric oxide synthas

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

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

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

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

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

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

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

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

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

151 Microglial cell function is implicated in the etiology o

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

153 The presence of activated microglial cells has been noted in autopsy specimens of

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

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

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

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

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

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

160 in a mouse microglial cell line and primary microglial cells in association with increased cell migr

161 We also found that CNS-resident microglial cells in both the resting and activated state

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

163 llular calcium homeostasis in mouse cortical microglial cells in culture.

164 basis for comparison with the morphology of microglial cells in disease and injury models where they

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

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

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

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

169 in vitro utility of PrP(Sc)-permissive sheep microglial cells in investigating the biology of natural

170 to P2X(4) and P2X(7) receptors expressed by microglial cells in neuropathic and inflammatory pain; a

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

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

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

174 Microglial cells in the brain tumor microenvironment are

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

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

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

178 These data showing "resting" Iba-1 labeled microglial cells in the normal adult rat dentate gyrus p

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

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

181 Because mGluR5 is expressed by microglial cells in the rat spinal cord, such effects ma

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

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

184 Here, we examined whether microglial cells in the thalamus contribute to the modul

185 NK cells rapidly formed synapses with human microglial cells in which perforin had been polarized to

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

187 protection was correlated with activation of microglial cells indicated by the up-regulation of MHC I

188 lin-specific T cells into CNS, activation of microglial cells, inflammation of CNS, dysfunction of lo

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

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

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

192 Because mFPR2 in microglial cells is regulated by proinflammatory stimula

193 , we report that the oxidative burst of BV-2 microglial cells leads to oxidation or nitrosylation of

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

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

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

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

198 ne, induced mFPR2 mRNA expression in a mouse microglial cell line and primary microglial cells in ass

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

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

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

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

203 when injected intrathecally and in the BV-2 microglial cell line when applied in vitro.

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

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

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

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

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

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

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

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

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

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

214 teins in the neurons (but not astrocytes and microglial cells) of the striatum only.

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

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

217 Microglial cells or rats were treated with or without li

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

219 dentify an important mechanism through which microglial cells participate in the maintenance of Abeta

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

221 Thus, microglial cells play a previously unrecognized protecti

222 st that the activated A(2A)AR in the retinal microglial cells plays a major anti-inflammatory role in

223 Microglial cell-polarization correlated with maximal exp

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

225 to determine whether luteolin also regulates microglial cell production of a prototypic inflammatory

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

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

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

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

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

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

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

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

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

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

236 rvous system diseases, may profoundly affect microglial cell responses in the pathogenic process in w

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

238 ss was analyzed semi-quantitatively, whereas microglial cell size and levels of F4/80 immunoreactivit

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

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

241 Unstimulated microglial cells, subcultured from an astrocyte cocultur

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

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

244 In contrast, microglial cells support young neurons.

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

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

247 Microglial cells surround aggregated Abeta and are belie

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

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

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

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

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

253 y is associated with increased expression of microglial cells that are thought to participate in eith

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

255 auterine inflammation leads to activation of microglial cells that may be responsible for the develop

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

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

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

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

260 We report that the response of microglial cells to fibrillar forms of Abeta requires th

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

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

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

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

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

266 ted to reduce inflammatory responses and, in microglial cells, to promote phagocytosis.

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

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

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

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

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

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

273 rains were fixed, sectioned, and stained for microglial cells using biotinylated tomato lectin.

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

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

276 cells might edit resting and activated human microglial cells via killing in vitro.

277 so increased the endocytosis of Abeta(42) by microglial cells via mFPR2.

278 1beta from microglia, possibly by regulating microglial cell viability, and suggest an important alte

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

280 e effect of IFN-gamma on mFPR2 expression in microglial cells was dependent on activation of MAPK and

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

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

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

284 eptor (AR) subtypes expressed in rat retinal microglial cells were assessed by quantitative real-time

285 Additionally, microglial cells were frequently seen apposing the cell

286 Activated microglial cells were further identified as the predomin

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

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

289 ge, and increases in reactive astrocytes and microglial cells were observed in the hippocampal CA1 re

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

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

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

293 of nitric oxide (NO) production by activated microglial cells, which is a marker of classically activ

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

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

296 Treatment of microglial cells with 0.1 nM to 1 microM dieldrin for 24

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

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

299 eatment of primary murine microlgia and BV-2 microglial cells with luteolin inhibited LPS-stimulated

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