ライフサイエンスコーパス: RPE cell

1 RPE cells differentiated from these hiPSCs contained mor

2 RPE cells divide with greater variability, consistent wi

3 RPE cells grown as stable monolayers were exposed to 5%

4 RPE cells play critical roles in the maintenance of phot

5 RPE cells started migrating after the first day, and in

6 RPE cells were selectively destroyed by the line scannin

7 ubretinal drusenoid deposits and drusen, (2) RPE cell bodies, and (3) the choriocapillaris' vascular

8 irmed similar phenotypes, including abnormal RPE cells and late-onset photoreceptor cell loss.

9 Conditioned medium of inflammasome-activated RPE cells provided an additional priming effect that was

10 Finally, in aged RPE cells, TSPO expression was reduced and cholesterol e

11 lbino RPE cells at E13.5 but at E15.5 albino RPE cells have fewer small connexin 43 puncta, and a lar

12 rotein) is expressed in pigmented and albino RPE cells at E13.5 but at E15.5 albino RPE cells have fe

13 RPE markers Otx2 and Mitf similarly, albino RPE cells are irregularly shaped and have fewer melanoso

14 ppears loosely distributed within the albino RPE cells rather than tightly localized on the cell memb

15 better able to control bacillary growth and RPE cell survival is greater than that of THP-1 cells fo

16 situ hybridization reveals photoreceptor and RPE cell AdipoR1 expression, blunted in AdipoR1(-/-) mic

17 ar M tuberculosis was observed per THP-1 and RPE cells (0.45 and 0.35 M tuberculosis per RPE and THP-

18 eptors regulate VEGF expression in ChECs and RPE cells.

19 the activation of microglia/macrophages and RPE cells isolated from model mice as well as wild-type

20 Patient podocytes and RPE cells carrying disease-associated CFH genetic varian

21 ogy, normal morphology of outer segments and RPE cells, and no evidence of photoreceptor degeneration

22 ole in maintaining choroidal vasculature and RPE cells, implicating insufficiency in choroidal macrop

23 Preventing the endocytosis of C5b-9 by RPE cells led to structural defects in mitochondrial mor

24 rTK cleavage increased mostly POS binding by RPE cells.

25 VEGF production by RPE cells has been shown to be important in regulating a

26 The regulation of ECM remodeling by RPE cells is not well understood.

27 atRal and AP activation independently caused RPE cell death.

28 l to collect, seed, culture and characterize RPE cells from mice.

29 In conclusion, RPE cells consume multiple nutrients, including glucose

30 strikingly, phagocytosis of POS by cultured RPE cells was almost completely blocked by pharmacologic

31 on EMT and the fibrotic process in cultured RPE cells and further examined the preventive effect of

32 cible factor 1alpha (Hif-1alpha) in cultured RPE cells.

33 ly promote phagocytosis of shed POSs by D407 RPE cells.

34 ed RPE sheets and prevented dedifferentiated RPE cell proliferation and migration.

35 of contractile membranes by dedifferentiated RPE cells and suggest that adjunctive treatment targetin

36 of contractile membranes by dedifferentiated RPE cells on collagen I matrices.

37 location of beta-catenin in dedifferentiated RPE cells.

38 ess was verified in mice with Atg5-deficient RPE cells that showed evidence of disrupted lysosomal pr

39 The mechanism of Yap-dependent RPE cell type determination is reliant on both nuclear l

40 Mitochondrial DNA-depleted RPE cells demonstrated enhanced aerobic glycolysis by ex

41 in The Lancet of embryonic-stem-cell-derived RPE cell transplants indicate no serious adverse outcome

42 een of A2E-aged patient-specific iPS-derived RPE cell lines identified superoxide dismutase 2 (SOD2)-

43 applied to human embryonic stem cell-derived RPE cells and that the method is safe, efficient, and fu

44 ne approaches that utilise stem cell-derived RPE cells to treat conditions such as age-related macula

45 The hiPSC-derived RPE cells produce several AMD/drusen-related proteins, a

46 induced-pluripotent stem cell (iPSC)-derived RPE cells, particularly with regard to the complement pa

47 , Saini et al. (2017) show that iPSC-derived RPE cells from age-related macular degeneration patients

48 The RP2 patient fibroblasts and iPSC-derived RPE cells showed phenotypic defects in IFT20 localizatio

49 -dependent Cl(-) currents in patient-derived RPE cells by WT BEST1 gene supplementation.

50 posures produced by scanning laser destroyed RPE cells selectively, without damage to neural retina.

51 romotes a glycolytic shift in differentiated RPE cells and enhances resistance to oxidative damage.

52 dry AMD-like pathology, including disrupted RPE cell tight junctions, accumulation of RPE cell lipof

53 We find that dying RPE cells can activate the macrophage inflammasome and p

54 toxicity is more pronounced in dysfunctional RPE cells showing reduced IRAK3 gene expression.

55 eyes displayed replacement of dysfunctional RPE cells by hiPS-RPE cells.

56 Retinal pigment epithelial (RPE) cell death is a hallmark of age-related macular deg

57 Retinal pigment epithelial (RPE) cell death occurs early in the pathogenesis of age-

58 zed by extensive retinal pigment epithelial (RPE) cell death, and a cure is not available currently.

59 en implicated in retinal pigment epithelial (RPE) cell differentiation.

60 posits under the retinal pigment epithelial (RPE) cell layer is a pathognomonic feature of AMD.

61 we infected the retinal pigment epithelial (RPE) cell line, ARPE-19, with cell-associated VZV and co

62 at accumulate in retinal pigment epithelial (RPE) cells and are a hallmark of aging retina.

63 eased by primary retinal pigment epithelial (RPE) cells and iris pigment epithelial (IPE) cells stimu

64 versible loss of retinal pigment epithelial (RPE) cells and photoreceptors and can be associated with

65 us hiPSC-derived retinal pigment epithelial (RPE) cells are immune tolerated even in non-ocular locat

66 he lipofuscin of retinal pigment epithelial (RPE) cells are known to photodegrade to mixtures of alde

67 nd accumulate in retinal pigment epithelial (RPE) cells as lipofuscin; these fluorophores are implica

68 n protects human retinal pigment epithelial (RPE) cells from oxidative stress, a process involved in

69 nsition (EMT) of retinal pigment epithelial (RPE) cells is a critical step in the pathogenesis of PVR

70 gments (POSs) by retinal pigment epithelial (RPE) cells is critical to retinal homeostasis and shares

71 The adjacent retinal pigment epithelial (RPE) cells phagocytize and digest shed photoreceptor out

72 Retinal pigment epithelial (RPE) cells play an important role in formation of such f

73 egments (POS) by retinal pigment epithelial (RPE) cells requires several proteins, including MerTK re

74 mutant-TIMP3 in retinal pigment epithelial (RPE) cells showed increased secretion of bFGF and condit

75 hesized in human retinal pigment epithelial (RPE) cells that are oxygenated derivatives of VLC-PUFAs,

76 tiating cultured retinal pigment epithelial (RPE) cells towards a neuronal-like phenotype, but the un

77 g differentiated retinal pigment epithelial (RPE) cells with didanosine (ddI), which is associated wi

78 levels in human retinal pigment epithelial (RPE) cells, cells vulnerable in AMD, decrease with age.

79 r cells, but not retinal pigment epithelial (RPE) cells, rescued the retinal visual cycle and M-cone

80 ndition by using retinal pigment epithelial (RPE) cells, which are a crucial component of the outer b

81 cargo within the retinal pigment epithelial (RPE) cells.

82 eral membrane of retinal pigment epithelial (RPE) cells.

83 ion and death of retinal pigment epithelial (RPE) cells.

84 ss of underlying retinal pigment epithelial (RPE) cells.

85 ells (ChECs) and retinal pigment epithelial (RPE) cells.

86 al microvilli of retinal pigment epithelial (RPE) cells.

87 tina in-vivo and retinal-pigment-epithelial (RPE) cells in-vitro.

88 eral membrane of retinal-pigment-epithelial (RPE) cells, where it mediates uptake of iron by the neur

89 o lysosomes of retinal pigmented epithelial (RPE) cells acts to clear this harmful enzyme from the ex

90 cultured human retinal pigmented epithelial (RPE) cells and impairs lysosomal function.

91 Retinal pigmented epithelial (RPE) cells are essential for maintaining normal visual f

92 Differentiated retinal pigmented epithelial (RPE) cells have been obtained from human induced pluripo

93 ng produced by retinal pigmented epithelial (RPE) cells under different conditions simulating risk fa

94 e delivered to retinal pigmented epithelial (RPE) cells with a high efficiency compared with conventi

95 egeneration of retinal pigmented epithelial (RPE) cells, which has prompted exploration of the therap

96 pical aspects of retinal pigment epithelium (RPE) cells and contributes to a delayed c-wave response.

97 uller cells, and retinal pigment epithelium (RPE) cells and were visualized using confocal microscopy

98 Retinal pigment epithelium (RPE) cells are cultured on top of custom-made electrodes

99 Retinal Pigment Epithelium (RPE) cells generated from a patient with an inherited ma

100 migration of the retinal pigment epithelium (RPE) cells in age-related macular degeneration (AMD) usi

101 tion beneath the retinal pigment epithelium (RPE) cells is supposed to contribute the pathogenesis of

102 ein expressed in retinal pigment epithelium (RPE) cells that may have a key role in intercellular adh

103 In human retinal pigment epithelium (RPE) cells, the primary site for the fusion of optic fis

104 ncorporated into retinal pigment epithelium (RPE) cells.

105 nal support from retinal pigment epithelium (RPE) cells.

106 ulation in human retinal pigment epithelium (RPE) cells.

107 of human primary retinal pigment epithelium (RPE) cells.

108 tive stress-induced damage in an established RPE cell line (ARPE-19).

109 i were noticed in a subset of Cre-expressing RPE cells in aged heterozygous VMD2-Cre mice, whereas mo

110 ChIP with human fetal RPE cells shows that SOX9 and OTX2 also bind to the huma

111 human fetal RPE and polarized primary fetal RPE cells to validate the basic observation that sulinda

112 ion of C5b-9 by this route are essential for RPE cell survival.

113 hotoreceptor cells and NHE8 is important for RPE cell polarity and function.

114 tivation product C5a as a priming signal for RPE cells that allows for subsequent inflammasome activa

115 a-CDs to complex and remove LB deposits from RPE cells and provide crucial data to develop novel prop

116 ix molecules commonly found in deposits from RPE cells, in an AhR-dependent manner.

117 th green fluorescent protein-positive (GFP+) RPE cells was used to assess the efficacy of dasatinib i

118 tified that OR2W3 gene was expressed in HESC-RPE cell line.

119 placement of dysfunctional RPE cells by hiPS-RPE cells.

120 n of functional visual cycle enzymes in hiPS-RPE cells compared with that of isolated wild-type mouse

121 However, the visual (retinoid) cycle in hiPS-RPE cells has not been adequately examined.

122 osome formation also were documented in hiPS-RPE cells in vitro.

123 s was maintained during cell culture of hiPS-RPE cells, whereas expression of these same molecules ra

124 Together, our results show that hiPS-RPE cells can exhibit a functional visual cycle in vitro

125 Finally, when hiPS-RPE cells were transplanted into the subretinal space of

126 human induced pluripotent stem cell (hiPSC)-RPE cells from an individual carrying a homozygous c.158

127 This current is severely reduced in hiPSC-RPE cells derived from macular dystrophy patients with p

128 We found that the LCA16 hiPSC-RPE cells had normal morphology but did not express a fu

129 both control (unaffected) and patient hiPSC-RPE cells.

130 after lentiviral gene delivery to the hiPSC-RPE cells.

131 a novel autocrine/paracrine pro-homeostatic RPE cell signaling that aims to sustain photoreceptor ce

132 ese recent insights, it is still unclear how RPE cells die during the course of the disease.

133 However, RPE cells are better able to control bacillary growth an

134 the whole culture yielded a highly pure hPSC-RPE cell population that displayed many of the morpholog

135 d Pluripotent Stem Cells (iPSCs) and a human RPE cell line.

136 in in co-transfection experiments in a human RPE cell line.

137 In cultured human RPE cell line ARPE-19, expression of extrinsic JN up-reg

138 Abeta targets the RPE, we used primary human RPE cell cultures and demonstrated that OAbeta caused ce

139 of mitochondrial DNA in differentiated human RPE cells should be widely applicable for other studies

140 Using (13)C metabolic flux analysis in human RPE cells, we found that RPE has an exceptionally high c

141 bits CD4 T cell activation by infected human RPE cells.

142 ut there is no direct evidence in live human RPE cells to support this idea.

143 We found that incubation of primary human RPE cells and ARPE-19 cells with complement-competent hu

144 in vivo, and a protective role toward human RPE cells in vitro.

145 pression array analysis on A2E-treated human RPE cells and found up-regulation of four autophagy rela

146 developed and tested in the vitreous humor, RPE cell homogenates and intact RPE cells.

147 metabolism are radically altered in hypoxic RPE cells; these changes impact nutrient availability fo

148 ck of pigment in the RPE results in impaired RPE cell integrity and communication via gap junctions b

149 plement activation is strongly implicated in RPE cell dysfunction and loss in age-related macular deg

150 in normal subjects, adding great interest in RPE cell biology.

151 Acute activation of dynamin-1 in RPE cells by inhibition of GSK3beta accelerates CME, alt

152 To decipher the role of ERK1/2 in RPE cells, we conditionally disrupted the Erk1 and Erk2

153 detergent-insoluble ferritin accumulates in RPE cells and correlates temporally with microglial acti

154 MPO also disrupts lysosomal acidification in RPE cells, which coincides with nuclear translocation of

155 riming signal for inflammasome activation in RPE cells.

156 actively regulates its surface activation in RPE cells.

157 Indeed, knockout of AMPK in RPE cells using Clustered Regularly Interspaced Palindro

158 ro, inhibiting rotenone-induced autophagy in RPE cells elicits caspase-3 mediated cell death.

159 a) induction of complement factor B (CFB) in RPE cells.

160 We demonstrate in RPE cells that TSPO specific ligands promoted cholestero

161 implicated in several fibrotic diseases, in RPE cells in proliferative vitreoretinopathy.

162 suppress TNF-alpha-induced CFB expression in RPE cells in an AMPK-independent mechanism, and could be

163 In contrast, constitutive Otx2 expression in RPE cells prevents degeneration of photoreceptors in Otx

164 Surprisingly, upregulation of ferritin in RPE cells by exogenous iron in-vitro stimulated the rele

165 mplement cascade, is up-regulated by iron in RPE cells.

166 se (by half) of caveolin-1 protein levels in RPE cells in culture was sufficient to accelerate or imp

167 moved bidirectionally along microtubules in RPE cells, with kinesin-1 light chain 1 (KLC1) remaining

168 To clarify the role of miRNAs in RPE cells, we used two different mature RPE cell-specifi

169 asome activation in non-RPE cells but not in RPE cells promotes CNV.

170 AdipoR1 overexpression in RPE cells enhances DHA uptake, whereas AdipoR1 silencing

171 OPT2 mediate the uptake of these peptides in RPE cells.

172 tion protein expression, and permeability in RPE cells.

173 was recruited to maturing phagolysosomes in RPE cells in culture.

174 ice with a conditional knock-out of Rdh10 in RPE cells (Rdh10 cKO) displayed delayed 11-cis-retinal r

175 he data imply that phagocytosis receptors in RPE cells are sensitive to oxidative modification, raisi

176 o the pathological abnormalities reported in RPE cells studied from post-mortem tissues of affected m

177 mechanism for preventing oxidative stress in RPE cells and suggest that sulindac could be used therap

178 AnxA8 suppression in RPE cells via siRNA or administration of FR induced neur

179 ific ligands or by overexpression of TSPO in RPE cells.

180 with ER, Golgi and intracellular vesicles in RPE cells.

181 ean, and sum autofluorescence for individual RPE cells were measured (cellular autofluorescence [CAF]

182 mice are resistant to sodium iodate-induced RPE cell death.

183 potent inhibitor of oxidative stress-induced RPE cell death.

184 reous humor, RPE cell homogenates and intact RPE cells.

185 to differentiate pluripotent stem cells into RPE cells suitable for disease modelling and therapy dev

186 ll-trans-ROL uptake from photoreceptors into RPE cells through an as yet undefined mechanism.

187 d hypoxia-induced expression of CL-11 in iPS-RPE cells, and in the extracellular fluid.

188 both the R120X patient fibroblasts and iPSC-RPE cells.

189 , we rescued Kir7.1 channel function in iPSC-RPE cells derived from an affected individual.

190 P2X7R stimulation did not kill RPE cells but alkalinized lysosomes by 0.3 U.

191 Application of strategies to limit RPE cell loss may prove useful in eyes with neovascular

192 ne whether AnxA8 plays a role in maintaining RPE cell phenotype we directly manipulated AnxA8 express

193 s in RPE cells, we used two different mature RPE cell-specific Cre recombinase drivers to inactivate

194 HX2) are coexpressed in the nuclei of mature RPE cells, and that SOX9 acts synergistically with ortho

195 lts from a nonsense variant and so the MERTK-RPE cells were subsequently treated with two translation

196 d the features of albino and pigmented mouse RPE cells during the period of RGC neurogenesis (embryon

197 ARPE-19 and primary mouse RPE cells were cultured in the presence or absence of va

198 ing and the presence of large multinucleated RPE cells, suggesting defects in intercellular adhesion

199 a suggest that, epigenetically, adult murine RPE cells are a progenitor-like cell type.

200 usly developed to collect and culture murine RPE cells on Transwells as functional polarized monolaye

201 normalities were not noticed in Cre-negative RPE cells in VMD2-Cre or age-matched control mice.

202 el that NLRP3 inflammasome activation in non-RPE cells but not in RPE cells promotes CNV.

203 al pigment epithelium (RPE) or rather in non-RPE cells promotes CNV, (2) whether inflammasome activat

204 then used to find that Muller glia, but not RPE cells, are essential for this process.

205 ed RPE cell tight junctions, accumulation of RPE cell lipofuscin, basal laminar and linear-like depos

206 ssure region with concomitant acquisition of RPE cell fate.

207 ent reduced by 73% and 48% the LB content of RPE cell cultures and of eyecups obtained from Abca4-Rdh

208 rocess we performed a microarray analysis of RPE cells pre- and post-FR treatment, and observed a mar

209 lly in a zone corresponding to the apices of RPE cells, at the roots of the RPE microvilli, and at th

210 ts of the RPE microvilli, and at the base of RPE cells next to the Bruch's membrane.

211 din) was observed at the apices and bases of RPE cells.

212 The collection of RPE cells takes approximately 3 h, and the cultures mimi

213 ual function, and a rapid disorganization of RPE cells, ultimately leading to retinal degeneration.

214 (ADRD), and demonstrate that dysfunction of RPE cells alone is sufficient for the initiation of sub-

215 rowth factor-beta2(TGF-beta2)-induced EMT of RPE cells by deacetylating SMAD4.

216 Epithelial-mesenchymal transition (EMT) of RPE cells was assessed by expression of S100A4.

217 CC controlled VZV but not HSV-1 infection of RPE cells, suggesting that HSV-1 actively inhibits CD4 T

218 nd lymphocytic responses to VZV infection of RPE cells, thereby providing a useful platform for futur

219 eposited in both the extracellular matrix of RPE cells and aged donor BrM tissue.

220 ests that 2AI alters the lipid metabolism of RPE cells, enhancing the intracellular levels of palmito

221 The expected hexagonal mosaic of RPE cells was only sometimes seen in normal eyes, while

222 In Le-cre; Wls(fl/fl) mice, the numbers of RPE cells are reduced and this can explain, using the pr

223 Following priming of RPE cells, the NLRP3 inflammasome can be activated by va

224 y was performed to evaluate proliferation of RPE cells.

225 yap (yap1) mutants lack a subset of RPE cells and/or exhibit coloboma.

226 ficient for neuronal transdifferentiation of RPE cells and reveal an essential role for AnxA8 as a ke

227 Treatment of RPE cells with AnxA8 siRNA recapitulated exposure to FR,

228 ombined effect of atRal and AP activation on RPE cell viability.

229 However, their effect on RPE cells has not been fully elucidated.

230 d phosphoproteomic analysis of phagocytosing RPE cells, utilizing three different experimental models

231 2.5 and E15.5, although albino and pigmented RPE cells express RPE markers Otx2 and Mitf similarly, a

232 ve fewer melanosomes compared with pigmented RPE cells.

233 Primary cultures of porcine RPE cells were differentiated into polarized RPE monolay

234 he basal surface of cultured primary porcine RPE cells but disappears over 48 h without any discernab

235 polipoproteins secreted from primary porcine RPE cells.

236 Primary RPE cells from Mertk(-/-) mice also accumulated fluoresc

237 peed live imaging of polarized adult primary RPE cells and data from a mouse model of early-onset mac

238 ted AnxA8 expression in cultured and primary RPE cells using siRNA-mediated gene suppression, and ove

239 CFB expression in ARPE-19 and human primary RPE cells in a dose-dependent fashion.

240 t of differentiated ARPE-19 or human primary RPE cells with 200 uM ddI for 6-24 days was not cytotoxi

241 e cell line ARPE-19, cultured murine primary RPE cells, and RPE samples from live mice.

242 We used primary RPE cells from a mouse model of inherited MD due to a p.

243 inding was further corroborated with primary RPE cells and RPE explants.

244 ivity localizes to the nuclei of prospective RPE cells.

245 As shown here, sulindac can also protect RPE cells from chemical oxidative damage or UV light by

246 lammatory transcriptional events and protect RPE cells and PRC, and therefore have potential as a pos

247 nying uptake, both fusion proteins protected RPE cells from apoptosis, as indicated by reduced caspas

248 ed AhR activation, palmitoleic acid protects RPE cells from 4HNE-mediated stress, and light mediated

249 potent synthetic ligand of AhR that protects RPE cells in vitro from lipid peroxidation cytotoxicity

250 Efemp1(R345W) RPE cells recapitulate the basal deposit formation obser

251 at the time of silicone oil removal revealed RPE cells with intracellular silicone oil droplets, sing

252 atRal sensitizes RPE cells to AP attack, which may be mediated in part by

253 antitative and reproducible patient-specific RPE cell repair studies.

254 nhibited proliferation and EMT of stimulated RPE cells by down-regulating Wnt (beta-catenin, LEF1) an

255 urface modifications on oxidatively stressed RPE cells.

256 n clinical trials and can efficiently target RPE cells.

257 We conclude that RPE cells use the endocytic pathway to prevent the accum

258 degeneration; therefore, it is critical that RPE cells use molecular strategies to mitigate the poten

259 We have recently demonstrated that RPE cells die from necrosis in response to oxidative str

260 From a microarray analysis, we found that RPE cells express particularly high levels of the mitoch

261 r and colon), leading to the hypothesis that RPE cells, like hepatocytes, can produce beta-hydroxybut

262 Overall, our results indicate that RPE cells carrying the m.3243A > G mutation have a reduc

263 Our data show that RPE cells with constitutively high mTORC1 activity were

264 lthough in vitro studies have suggested that RPE cells can phagocytose emulsified oil droplets, this

265 The RPE cell cultures are suitable to study the biology of t

266 rol POS binding of integrin receptors at the RPE cell surface as a negative feedback loop.

267 hether EMP2 regulates VEGF expression in the RPE cell line, ARPE-19.

268 sion of alphaB results in a phenotype of the RPE cell that contains an increased number of vacuoles a

269 brane-bound complement regulator CD59 to the RPE cell surface inhibits MAC formation.

270 The RPE cells can also be manipulated to investigate molecul

271 This suggests that although the RPE cells are losing thickness and function, evidenced b

272 eir distal OS, which are phagocytosed by the RPE cells.

273 ction of TSPO in cholesterol efflux from the RPE cells.

274 that contribute to lipid accumulation in the RPE cells during aging and age-related degeneration.

275 NOS and Hsp70, late-phase IPC markers in the RPE cells.

276 d proliferation in approximately half of the RPE cells in treatment areas.

277 Since the RPE cells persist for the entire lifespan of an organism

278 based delivery systems were non-toxic to the RPE cells, chemically stable in porcine vitreous and del

279 rototypes (hydrophobic & hydrophilic) to the RPE cells.

280 ts but might also be useful in utilizing the RPE cells as mediators of drug delivery to intracellular

281 ial A2E and lipofuscin accumulation in their RPE cells but no retinal degeneration up to 12 months of

282 honeycomb pattern of RPE morphology in those RPE cells that stained for Cre.

283 lement pathway (AP) activation contribute to RPE cell death in both of these retinal disorders.

284 of reductive carboxylation may contribute to RPE cell death.

285 that the loss of miRNAs also contributes to RPE cell death and loss of visual function and could aff

286 due to DICER1 deficiency also contributes to RPE cell death.

287 ccumulation, and IL-18 up-regulation lead to RPE cell death via activation of Caspase-8 through a Fas

288 retinal hyperreflective foci attributable to RPE cells and lipid-filled cells of monocyte origin.

289 lective foci as seen on SD OCT correlated to RPE cells on histologic examination.

290 above 7.5, proved to be remarkably toxic to RPE cells with or without trypan blue.

291 mine (A2E), are thought to be transferred to RPE cells primarily through phagocytosis of the photorec

292 ssion in RPE by half, 50% of the transfected RPE cells were selectively destroyed by microsecond expo

293 TSPO-/- RPE cells also had significantly increased production of

294 umulation were markedly increased in TSPO-/- RPE cells.

295 nd HC-HA/PTX3 were not toxic to unstimulated RPE cells.

296 ximately 3 h, and the cultures mimic in vivo RPE cell features within 1 week.

297 transiently adhered to the RPE before which RPE cells appeared dysmorphic.

298 sm of RPE-retina metabolic coupling in which RPE cells metabolize fatty acids to produce beta-HB, whi

299 Next their interaction with RPE cells was evaluated under oxidative stress.

300 2 than MMP-9 in their stimulated state, with RPE cells producing higher amounts of MMPs than IPE cell