ライフサイエンスコーパス: microglia

1 R4 in the NAc core is primarily expressed on microglia.

2 infiltrating macrophages and resident brain microglia.

3 ne and inhibited MMP-9 activation in primary microglia.

4 mmasome-dependent formation of ASC specks in microglia.

5 tion of inflammation-related genes linked to microglia.

6 d by classically activated neuroinflammatory microglia.

7 ffects of lysophosphatidylcholine (LPC) upon microglia.

8 and functional properties of brain-isolated microglia.

9 opsonize the live cells for phagocytosis by microglia.

10 ammatory signaling is reduced in CX3CR1(-/-) microglia.

11 ations, including phagocytic macrophages and microglia.

12 tive oxygen species (ROS) in macrophages and microglia.

13 re of H/H-N/N-exposed WT, but not TLR4(-/-), microglia.

14 mouse brains with fluorochrome expression in microglia.

15 ike receptor 4 (TLR4) localized primarily on microglia.

16 neuronal cell types were detected, including microglia.

17 could aid in the restoration of homeostatic microglia.

18 triggered earlier astrocytosis and reactive microglia.

19 sion of activating FcgammaRs on M1-polarized microglia.

20 n-dependent silencing of Rgs10 expression in microglia.

21 transmembrane molecule uniquely expressed in microglia.

22 lammatory gene expression in macrophages and microglia.

23 Genetic ablation of Panx1 in microglia abolished the spinal synaptic facilitation and

24 % of the total TAM population, with resident microglia accounting for the approximately 15% remaining

25 During ageing, microglia acquire a phenotype that may negatively affect

26 vidence indicates that IFNgamma can increase microglia activation and induce Abeta production.

27 Because low-level sustained microglia activation can lead to abnormal responses to a

28 Although microglia activation has been noted in all types of psyc

29 We found microglia activation in normal white matter of controls

30 Priming microglia with LPS induced greater microglia activation in the PAG of females compared with

31 served in females is the result of increased microglia activation in the periaqueductal gray (PAG), a

32 PA in switching Araf protein isoforms during microglia activation, impacting production of downstream

33 eliver drug-loaded nanoparticles directly to microglia after TBI.

34 However, the precise mechanisms by which microglia alter the course of AD neuropathology remain p

35 HMGB1 messenger RNA in enriched hippocampal microglia, an effect that persists for up to 6 weeks aft

36 1 receptor kinase signaling PLX5622 depleted microglia and alleviated the catatonic symptoms of Cnp m

37 increase in the expression of galectin-3 in microglia and also an increase in the released form of g

38 In the OB, we observed activation of microglia and astrocytes and decreased expression of tyr

39 Finally, we confirm that plaque-localised microglia and astrocytes are reduced in ABX-exposed mice

40 Drugs of abuse can activate microglia and astrocytes through signaling at innate imm

41 ield a marked accumulation of astrocytes and microglia and decrease of neurons for the same period.

42 g memory was closely correlated with reduced microglia and endothelial adhesion molecules.

43 ernalization and dissolution of AgNPs within microglia and formation of non-reactive silver sulphide

44 may also induce aging-like sensitization of microglia and increase reactivity to secondary challenge

45 Only concurrent double depletion of microglia and infiltrated macrophages slightly, but sign

46 injury (SCI), the innate immune response of microglia and infiltrating macrophages clears up cellula

47 sponse involving both activation of resident microglia and infiltration of CD4(+) and CD8(+) T lympho

48 Thus, microglia and low-grade inflammation of myelinated tract

49 is upregulation is associated with increased microglia and macrophage populations in the cortical les

50 Glioma-associated microglia and macrophages (GAM), which infiltrate high-g

51 Microglia and macrophages accumulate at the sites of act

52 In later stages, the microglia and macrophages in active lesions changed to a

53 Our results highlight an important role for microglia and neuroinflammation during congenital ZIKV p

54 neuronal defects induced by defective Hoxb8-microglia and neuronal dysfunctions directly generated b

55 Microglia and other tissue-resident macrophages within t

56 yeloid compartment that includes parenchymal microglia and perivascular macrophages, as well as choro

57 t includes activation of the tissue-resident microglia and recruitment of blood-derived macrophages a

58 d by migration and proliferation of resident microglia and recruitment of circulating monocytes.

59 s, which was associated with fewer activated microglia and reduced CGRP expression in the dorsal horn

60 lls, and choroid plexus cells), most notably microglia and/or macrophages.

61 associated protein (RAP), robustly activated microglia, and its activity was attenuated in LRP1-defic

62 e brain, TREM2 is predominately expressed on microglia, and its association with AD adds to increasin

63 romoted the anti-inflamed M2 polarization in microglia, and microglial exosomal miR-124-3p inhibited

64 showed that the distribution of astrocytes, microglia, and neurons became uniform from 2-12 wk, wher

65 t endogenous RGS10 is present in spinal cord microglia, and RGS10 protein levels are suppressed in th

66 tory cytokine tumor necrosis factor-alpha in microglia, and the recruitment of the nuclear factor-kap

67 Microglia are a type of macrophage that function as resi

68 Activated microglia are a universal feature of ALS/FTD pathology;

69 Microglia are activated by any type of pathologic event

70 Translocator protein density increases when microglia are activated during neuroinflammation and the

71 Microglia are brain-resident myeloid cells that mediate

72 Microglia are essential for CNS homeostasis and innate n

73 Given microglia are implicated in neurodegenerative disorders

74 are critical in stroke pathophysiology, and microglia are key cellular effectors in the CNS response

75 Therefore, microglia are not essentially involved in RGC degenerati

76 Microglia are perpetually engaged in a mutual interactio

77 primary source of proinflammatory cytokines, microglia are pivotal mediators of neuroinflammation and

78 resolution phase, excess disease-associated microglia are removed by a dual mechanism of cell egress

79 Microglia are resident cells of the brain that regulate

80 These results demonstrate that PAG microglia are sexually dimorphic in both basal and LPS-i

81 ondrial dynamics and associated signaling in microglia are still poorly understood.

82 Microglia are the intrinsic immune sentinels of the cent

83 Microglia are the main resident macrophage population of

84 Microglia are the resident macrophages of the central ne

85 which arise from multiple progenitor pools, microglia arise from yolk sac progenitors and are widely

86 tify activation of the MAP kinase pathway in microglia as a cause of neurodegeneration and this offer

87 includes neurons, astrocytes, pericytes, and microglia as well as the blood vessels themselves.

88 but emerged in various cell types, including microglia, astrocytes and vascular endothelial cells.

89 Although RGS10 is normally expressed in microglia at high levels, expression is silenced in vitr

90 Microglia belong to a lineage of adult tissue-resident m

91 Microglia, brain immune cells with ramified and dynamica

92 hanges in TSPO levels were not restricted to microglia but emerged in various cell types, including m

93 not universally conform to the phenotype of microglia, but preferentially express immunosuppressive

94 eased P2X7R function was blocked in cultured microglia by PP2, a Src family protein tyrosine kinase i

95 etifoxine was abolished in mice depleted of microglia by using a colony-stimulating factor 1 recepto

96 g on their activation state and environment, microglia can be beneficial or detrimental.

97 Activated microglia can phagocytose dying, stressed, or excess neu

98 Microglia can strongly influence the pathologic outcome

99 upregulated in activated glia (predominantly microglia), can be measured as an indication of neuroinf

100 to be microglia, we suggested that defective microglia cause the neuropsychiatric disorder.

101 d iNOS and COX-2 expression in the BV2 mouse microglia cell line and inhibited MMP-9 activation in pr

102 a subtype-dependent increase in macrophages/microglia cells upon disease recurrence.

103 secretion of proinflammatory mediators from microglia cells, ultimately rescuing neurons from death.

104 Our results suggest that microglia change to a more swollen, 'activated' shape wi

105 ndent manner that involves downregulation of microglia checkpoints, followed by activation of a Trem2

106 ry cytokine interleukin-1beta from activated microglia, consistent with K(+) loss being needed for in

107 e demonstrate that periaqueductal gray (PAG) microglia contribute to the sexually dimorphic effects o

108 evidence also indicate that dysregulation of microglia contributes to the pathogenesis of neurodegene

109 Microglia control excitatory synapses, but their role in

110 Our findings suggest that microglia control MG responsiveness to photoreceptor los

111 Microglia coordinate various functions in the central ne

112 dated this hypothesis in primary fetal sheep microglia cultures re-exposed to LPS in presence of a se

113 5H and Cst7, a marker for disease-associated microglia (DAM), which encodes an endosomal/lysosomal ca

114 blation in monocytes/macrophages, but not in microglia, delayed the onset of EAE in challenged animal

115 re, in vitro analysis using cultured primary microglia demonstrated the role of interferon (IFN)gamma

116 ress Rgs10 transcription in BV-2 and primary microglia, demonstrating that HDAC enzymes are required

117 Moreover, identification of IFN-driven microglia-dependent synapse loss, along with microglia t

118 rmally inhibited by abGCs, were increased in microglia-depleted mice.

119 Microglia depletion significantly lowered spine density

120 by astrocytes was significantly delayed upon microglia depletion, spontaneous and LI-induced axon reg

121 Quinolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plethora of fun

122 nd activate regulatory elements that control microglia development and their responses to internal an

123 hat Panx1 activation drives ATP release from microglia during morphine withdrawal and that degrading

124 Region-specific phenotypes of BG microglia emerged during the second postnatal week and w

125 Mice lacking TDP-43 in microglia exhibit reduced amyloid load in a model of Alz

126 Microglia exhibit two modes of motility: they constantly

127 noted within the PAG of male or female rats, microglia exhibited a more "activated" phenotype in fema

128 LPS-activated microglia exhibited a sialidase activity that desialylat

129 The microglia exhibited an activated M1 phenotype consistent

130 Microglia expansion required the adequate presence of fa

131 rferon (IFN)-stimulated gene response within microglia exposed to ischemia/reperfusion in both in vit

132 e-dependent induction of NLRP3 expression in microglia exposed to Tat compared with control.

133 Our results show that resident spinal microglia express the G-CSF receptor and that G-CSF sign

134 k, we investigated the specific responses of microglia following ICH with the aim of identifying path

135 sion and assembly of the immunoproteasome in microglia following interferon-gamma exposure.

136 0 proximal promoter are deacetylated in BV-2 microglia following LPS activation, and HDAC1 associatio

137 g and inhibitory FcgammaRs on brain-resident microglia following murine cytomegalovirus (MCMV) infect

138 er, we highlight the complexity of targeting microglia for therapeutic intervention in neurodegenerat

139 erized the transcriptional profiles of adult microglia from APP/PS1 mice and identified a role for RI

140 ges: (1) an early mobilization of endogenous microglia from the inner retina to the RPE layer, follow

141 f a CSF1R inhibitor eliminated virtually all microglia from the visual system, whereas macrophages we

142 or of proinflammatory cytokine production in microglia, functioning as an important neuroprotective f

143 ted mixed primary cultures of astrocytes and microglia had higher levels of MMP2 and MMP9 activity th

144 APOE-mediated neurodegenerative microglia had lost their tolerogenic function.

145 proportions of blood-derived macrophages and microglia have been poorly quantified in clinical sample

146 In recent years, retinal microglia have been shown to influence vascular branchin

147 These iPSC-derived microglia have the phenotype, gene expression profile an

148 r physiological microglial function, and how microglia help to maintain tissue homeostasis in the CNS

149 The lifespan of brain microglia, however, remains uncertain, and reflects conf

150 response by suppressing the accumulation of microglia (Iba-1+) and lymphocytes (CD45+) into the graf

151 d CHIT1 staining colocalised with markers of microglia (IBA1) and macrophages (CD68).

152 e clearly define the mechanisms that control microglia identity and function in health and disease.

153 studies have demonstrated the importance of microglia in AD pathogenesis.

154 Here, we find that microglia in AD patients carrying TREM2 risk variants an

155 ntly, the heightened inflammatory profile of microglia in aging is associated with a 'sensitized' or

156 tudies have underscored the emerging role of microglia in Alzheimer's disease (AD) pathogenesis.

157 e ISF, illustrating a novel role for CR3 and microglia in brain Abeta metabolism and defining a poten

158 To clarify the role of microglia in brain homeostasis and disease, an understan

159 the function, as well as the dysfunction, of microglia in disorders of the CNS.

160 acilitate efforts to understand the roles of microglia in human brain diseases.

161 that DLG4 (PSD95) protein is synthesised by microglia in immature mouse and human, developmentally r

162 with accumulation of ERK-activated amoeboid microglia in mice, and is also observed in human patient

163 This could reflect that activated microglia in mild cognitive impairment initially may ado

164 oproteasome levels are elevated in activated microglia in models of stroke, infection and traumatic b

165 or inhibitor PLX5622 specifically eliminated microglia in murine retinae and optic nerves with high e

166 ha7nAChR agonists in early re-programming of microglia in neonates exposed to in utero inflammation v

167 The role of microglia in neurodegenerative diseases has been controv

168 ia/macrophages was significantly reduced and microglia in part converted to a P2RY12+ phenotype.

169 blood adopt the phenotype of brain-resident microglia in pre-treatment gliomas.

170 neuroimaging data to investigate the role of microglia in preterm white matter damage.

171 Rgs10 expression is dynamically regulated in microglia in response to multiple signals.

172 revented the increase in number of activated microglia in the ARC, the expression of the proinflammat

173 Proliferation and activation of microglia in the brain, concentrated around amyloid plaq

174 , which might explain the disparate roles of microglia in the development and progression of AD patho

175 dy to Mac1, we demonstrate a causal role for microglia in the development, but not maintenance, of mo

176 mic yet discrete self-organization of mature microglia in the healthy and diseased CNS.

177 These findings demonstrate that microglia in the healthy brain exhibit a spectrum of dis

178 mporaneously, diverse roles are emerging for microglia in the healthy brain, from sculpting developin

179 t-induced obese mice, persistently activated microglia in the MBH hypersecrete TNFalpha that in turn

180 hemistry to study beta-amyloid and activated microglia in the mouse brain tissue.

181 by an increase in the proportion of IBA1(+) microglia in the NAc that were immunopositive for activi

182 ally, we report that increased activation of microglia in the PAG contributes to the attenuated respo

183 By selectively ablating microglia in the spinal cord using a saporin-conjugated

184 in the visual cortex.SIGNIFICANCE STATEMENT Microglia in the visual cortex respond to monocular depr

185 e chronic phase of TBI to treat cultured BV2 microglia in vitro The microglial exosomes were collecte

186 o-inflammation model in mice and in cultured microglia in vitro.

187 of beta2-adrenergic receptors, and activated microglia in wt mice in vivo Thus, most soluble Abeta as

188 ammatory (M2) activation of CNS macrophages (microglia) in WNV-infected SCSC while inhibiting the exp

189 ignature, were abundantly expressed in human microglia, including TLR, Fcgamma and SIGLEC receptors,

190 When activated, microglia increase the expression of translocator protei

191 not of mice lacking IFN-I receptor on their microglia, induces an ageing-like transcriptional microg

192 Microglia, innate immune cells of the brain, and astrocy

193 Overall, our work uncovers a DRG neuron-microglia interaction that responds to G-CSF by engaging

194 id not affect the recruitment of macrophages/microglia into lesions, suggesting that creatine affects

195 manner, mediating increased infiltration of microglia into the subventricular zone of both FIP200hGF

196 napses and neural progenitor cells (NPCs) by microglia is critical for the development and maintenanc

197 hat mitochondrial fission/fusion in reactive microglia is differentially regulated from that in monoc

198 Dysfunction of microglia is known to play an important role in Alzheime

199 mitochondrial fission and fusion in reactive microglia is mediated by distinct signaling under inflam

200 of Transcription (Tat) protein can activate microglia is thus of paramount importance.

201 present gene expression profiles of purified microglia isolated at autopsy from the parietal cortex o

202 Using primary cultures of microglia isolated from mouse brains, we demonstrated th

203 Does the Hoxb8 mutation in microglia lead to neural circuit dysfunctions?

204 k requires production of prostaglandin E2 by microglia, leading to the activation of neuronal EP2 rec

205 models of these mechanisms by reprogramming microglia-like cells from peripheral blood mononuclear c

206 Microglia lose their amyloid-beta-clearing capabilities

207 patients with ALS may reflect the extent of microglia/macrophage activation in the white matter of t

208 stimulation of the innate immune system and microglia/macrophage activation via Toll-like receptor 9

209 aft model of GBM, C16 treatment overcame the microglia/macrophage barrier, thereby facilitating tumor

210 Glioma-associated microglia/macrophages (GAM) were identified as TSPO and

211 to monitor the effect of therapies targeting microglia/macrophages activation after TBI.

212 IR-induced microglia/macrophages associate with apoptotic retinal n

213 .T1 was also highly expressed by neurons and microglia/macrophages at 7 d after injury and declined b

214 Microglia/macrophages comprising approximately 40% of a

215 the microenvironment created by CX3CR1(-/-) microglia/macrophages enhances NG2 cell responses, axon

216 We show that IR leads to activation of microglia/macrophages indicated by migration and prolife

217 rate that while acute HIV infection of human microglia/macrophages results in massive apoptosis, a sm

218 In inactive lesions, the density of microglia/macrophages was significantly reduced and micr

219 tenuates glutamate synthesis in HIV-infected microglia/macrophages, offering therapeutic potential fo

220 lti-focal inflammation mediated by activated microglia/macrophages.

221 nduces Il4 expression and M2 polarization of microglia/macrophages.

222 aling, dynamic regulation of RGS10 levels in microglia may be an important mechanism to tune inflamma

223 l et al. present an underlying mechanism for microglia-mediated elimination of virally transduced cel

224 ated TrkA signaling is a potent regulator of microglia-mediated inflammation in a Jmjd3-dependent man

225 Here we show that DHEA reduces microglia-mediated inflammation in an acute lipopolysacc

226 indings provide additional evidence that the microglia-mediated innate immune response contributes di

227 ther, our data show that TGF-beta1 modulates microglia-mediated neuroinflammation after ICH and promo

228 ite matter abnormalities, extensive gliosis, microglia-mediated neuroinflammation, and an expansion o

229 Thy1-GFP-M mice were used to assess microglia-mediated neuronal remodeling and dendritic spi

230 Microglia (MG), a heterogeneous population of phagocytic

231 Overall, our data suggest that dysfunctional microglia might play a causative role in the pathogenesi

232 Microglia morphology and DAMP signaling in enriched rat

233 s revealed diverse and widespread changes to microglia morphology in the cortex post-mFPI.

234 Microglia morphology was quantified from histological se

235 onocyte-derived macrophages and the ramified microglia of normal white matter in myelin disease model

236 icroglia transcriptome and limiting Mef2C, a microglia 'off' signal.

237 We describe here the diversity of microglia phenotypes and their responses in health, agin

238 ranscriptional mechanisms that specify human microglia phenotypes are largely unknown.

239 Microglia play a pivotal role in the maintenance of brai

240 As the immune-competent cells of the brain, microglia play an increasingly important role in maintai

241 Here, we argue that microglia play an overall neuroprotective role in prion

242 Microglia play critical roles in brain development, home

243 Microglia play critical roles in tissue homeostasis and

244 Microglia play essential roles in central nervous system

245 Microglia play important roles in perinatal neuro- and s

246 after preterm birth.Inflammation mediated by microglia plays a key role in brain injury associated wi

247 may be at least partly mediated by deficient microglia polarization toward amyloid deposits, resultin

248 were cell-type specific and irrespective of microglia polarization.

249 lts suggest that chronic sleep loss, through microglia priming, may predispose the brain to further d

250 Finally, we find that mature microglia rapidly lose signature gene expression after i

251 We found that LPS-activated BV-2 microglia rapidly released Gal-3, which was blocked by c

252 findings implicating genetic variants of the microglia receptor, triggering receptor expressed on mye

253 We further demonstrate that microglia regulate the activity-dependent plasticity of

254 Microglia regulate the brain microenvironment by sensing

255 We conclude that activated microglia release Gal-3 and a neuraminidase that desialy

256 ing Nrp1 in either peripheral macrophages or microglia reprograms their phenotype and their pathogeni

257 pecialized gene expression profile of mature microglia requires continuous instructive signaling from

258 udy narrows the search for understanding how microglia respond to active synapse modification in the

259 cular basement membrane and demonstrate that microglia respond to the mural basement membrane in an i

260 literature about the impact of lifestyle on microglia responses and discuss treatment options that m

261 isualize neutrophil, macrophage, and retinal microglia responses to induced rod photoreceptor apoptos

262 erved calcium channel-independent effects on microglia, resulting in apoptosis.

263 ific transcriptional profiling revealed that microglia selectively enhanced CCL2 expression, while mo

264 esulting from CSE-mediated H2S production in microglia, sequesters Ag(+) ions released from AgNPs, si

265 Microglia serve as brain macrophages but are distinct fr

266 data show that genetic deletion of CX3CR1, a microglia-specific chemokine receptor, promotes recovery

267 dependent transcriptional network specifying microglia-specific programs of gene expression and facil

268 escence for glial fibrillary acidic protein, microglia-specific proteins Iba1 and CD68, and phosphory

269 ing adapter molecule 1+ immunoreactivity for microglia, suggesting chronic inflammation did not cause

270 ity, enhances basal Rgs10 expression in BV-2 microglia, suggesting that Rgs10 expression is dynamical

271 This microglia-synapse cross talk requires production of pros

272 significantly more bioactive on synapses and microglia than the HMW species from which they are deriv

273 kDa (TSPO) is overexpressed in the activated microglia that surround the beta-amyloid plaques.

274 icularly evident in hematopoietic cells with microglia, the brain-resident macrophage population bein

275 Although anesthetics appear to activate microglia, the increased uptake of dendrimer nanoparticl

276 S injury.SIGNIFICANCE STATEMENT The roles of microglia, the phagocytosing cells of the CNS, and invad

277 Microglia, the resident macrophages of the CNS, engage i

278 ances in our understanding of the biology of microglia, their contribution to homeostasis, and their

279 ransduced cells triggers their engulfment by microglia through TAM receptor-dependent mechanisms.

280 The persistence of individual microglia throughout the mouse lifespan provides an expl

281 This Review highlights the contribution of microglia to ALS/FTD pathogenesis, discusses the connect

282 thermore, we show that type I IFN stimulates microglia to become reactive and engulf neuronal and syn

283 lation and inflammatory responses of primary microglia to classic inflammatory stimuli.

284 brain impedes cognitive ability by altering microglia transcriptome and limiting Mef2C, a microglia

285 microglia-dependent synapse loss, along with microglia transcriptome data, connects CNS lupus with ot

286 We describe a novel microglia type associated with neurodegenerative disease

287 This unique microglia-type has the potential to restrict neurodegene

288 While proliferation of resident neocortical microglia under homeostatic conditions was low, microgli

289 ly to photo-toxicity, in that astrocytes and microglia undergo morphological changes, while in develo

290 d phagocytosis of primary neurons by primary microglia was also blocked by inhibition of MerTK.

291 t label with Hoxb8 cell lineage appear to be microglia, we suggested that defective microglia cause t

292 d DAMP signaling in enriched rat hippocampal microglia were examined during the development and expre

293 nditions, we found that neocortical resident microglia were long-lived, with a median lifetime of wel

294 no overall sex differences in the density of microglia were noted within the PAG of male or female ra

295 acologically or by gene knockout depolarizes microglia, which decreases microglial ramification and t

296 n addition, understanding AgNP processing by microglia will allow better prediction of their long ter

297 cetylcholine receptor (alpha7nAChR) in fetal microglia will augment their neuroprotective transcripto

298 Treatment of microglia with a metalloproteinase inhibitor inhibited L

299 Priming microglia with LPS induced greater microglia activation

300 EM2) is a transmembrane protein expressed on microglia within the brain.