ライフサイエンスコーパス: RPE cell

1 RPE cell-induced MDSCs were adoptively transferred into

2 RPE cells differentiated from these hiPSCs contained mor

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

4 RPE cells induce the differentiation of MDSCs from bone

5 RPE cells induced the differentiation of MDSCs.

6 RPE cells play critical roles in the maintenance of phot

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

8 RPE cells were selectively destroyed by the line scannin

9 RPE cells were treated with atRal and then incubated wit

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

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

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

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

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

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

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

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

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

19 control immune reactions in the retina, and RPE cell-induced MDSCs should be further investigated as

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

21 eptors regulate VEGF expression in ChECs and RPE cells.

22 xpression and protein secretion in ChECs and RPE cells.

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

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

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

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

27 rTK cleavage increased mostly POS binding by RPE cells.

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

29 atRal and AP activation independently caused RPE cell death.

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

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

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

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

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

35 uced activation of Wnt signaling in cultured RPE cells.

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

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

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

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

40 location of beta-catenin in dedifferentiated RPE cells.

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

42 induce MDSC differentiation, PD-L1-deficient RPE cells and blocking antibodies against TGF-beta, CTLA

43 PD-L1-deficient RPE cells induced MDSC differentiation as efficiently as

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

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

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

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

48 INTERPRETATION: The hESC-derived RPE cells showed no signs of hyperproliferation, tumorig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 rvous system and retinal pigment epithelial (RPE) cells in response to oxidative stress, which activa

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

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

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

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

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

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

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

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 al microvilli of retinal pigment epithelial (RPE) cells.

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

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

84 al from adjacent retinal pigment epithelial (RPE) cells.

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

86 eral membrane 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 Differentiated retinal pigmented epithelial (RPE) cells have been obtained from human induced pluripo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 detachments consisted predominantly of GFP+ RPE cells.

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

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

116 These features are seen in Hfe(-/-) RPE cells as well as in Hjv(-/-) RPE cells, providing a

117 pression of Slc5a8 was decreased in Hfe(-/-) RPE cells, but treatment with a DNA methylation inhibito

118 hiPS-RPE cells appeared morphologically similar to mpRPE cell

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

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

128 iferative phenotype of Hfe(-/-) and Hjv(-/-) RPE cells.

129 in Hfe(-/-) RPE cells as well as in Hjv(-/-) RPE cells, providing a molecular basis for the hyperprol

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

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

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

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

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

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

136 we show that a subpopulation of adult human RPE cells can be activated in vitro to a self-renewing c

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

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

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

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

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

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

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

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

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

146 rea, possibly resulting from a difference in RPE cell shape.

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

148 CTLA-2alpha were not measurably involved in RPE cell-induced MDSC differentiation, whereas IL-6 was

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

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

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

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

153 riming signal for inflammasome activation in RPE cells.

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

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

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

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

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

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

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

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

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

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

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

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

166 ecular network controlled in vivo by Otx2 in RPE cells.

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

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

169 tion protein expression, and permeability in RPE cells.

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

171 in vitro, pro-angiogenic VEGF production in RPE cells by PCR and ELISA, and for inhibition of choroi

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

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

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

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

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

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

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

179 Ectopic ataxin-1 expression induced RPE cell apoptosis, which was abrogated by 100 nm docosa

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

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

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

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

184 be used as a predictor for how well the iPS-RPE cells will function in vivo.

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

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

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

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

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

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

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

192 and primary wild-type and Gpr109a(-/-) mouse RPE cells were exposed to TNF-alpha in the presence or a

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

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

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

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

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

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

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

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

201 wever, blocking IL-6 reduced the efficacy of RPE cell-induced MDSC differentiation.

202 Finally, adoptive transfer of RPE cell-induced MDSCs suppressed IRBP-specific T-cell r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 ntense healing reaction and proliferation of RPE cells than previously characterized in rodent studie

218 y was performed to evaluate proliferation of RPE cells.

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

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

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

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

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

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

225 2.5 and E15.5, although albino and pigmented RPE cells express RPE markers Otx2 and Mitf similarly, a

226 ve fewer melanosomes compared with pigmented RPE cells.

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

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

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

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

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

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

233 on and secretion of IL-6 and Ccl2 in primary RPE cells from Gpr109a(-/-) mice, confirming that the ob

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

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

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

237 ivity localizes to the nuclei of prospective RPE cells.

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

239 tylation, or expression were able to protect RPE cells from apoptosis.

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

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

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

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

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

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

246 Similarly, RPE cells from hemojuvelin (Hjv)-knockout mice, another

247 sity of the phagocytosis receptors on single RPE cells were measured using flow cytometry.

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

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

250 urface modifications on oxidatively stressed RPE cells.

251 n clinical trials and can efficiently target RPE cells.

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

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

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

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

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

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

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

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

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

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

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

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

264 The RPE cells can also be manipulated to investigate molecul

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

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

267 ut indicates that the additional iron in the RPE cells does not result from loss of ferroxidases in t

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

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

270 binding and internalization dynamics of the RPE cells.

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

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

273 ron accumulation and transfer of iron to the RPE cells.

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

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

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

277 These RPE cell-induced MDSCs significantly inhibited T-cell pr

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

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

280 of reductive carboxylation may contribute to RPE cell death.

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

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

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

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

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

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

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

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

289 Trypsinization of treated RPE cells results in the release of bound POS.

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

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

292 differentiation as efficiently as wild-type RPE cells, and neutralizing TGF-beta or CTLA-2alpha did

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

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

295 of MDSCs could be another mechanism by which RPE cells control immune reactions in the retina, and RP

296 To explore the mechanism by which RPE cells induce MDSC differentiation, PD-L1-deficient R

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

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

299 2 than MMP-9 in their stimulated state, with RPE cells producing higher amounts of MMPs than IPE cell

300 yes had the same surgical procedures without RPE cell injection.