ライフサイエンスコーパス: retinal cell

1 al tumors can arise from an undifferentiated retinal cell.

2 vel GABA-mediated excitation within a single retinal cell.

3 S1, regulates ERK signaling and apoptosis in retinal cells.

4 rvival and integration of hESC-derived donor retinal cells.

5 in mouse and zebrafish resulted in death of retinal cells.

6 xidase activity in the retina or in cultured retinal cells.

7 modulated autophagosome formation in ARPE19 retinal cells.

8 L) seems to be ubiquitously expressed in all retinal cells.

9 ng the genesis, differentiation and death of retinal cells.

10 wn-regulate PPARalpha expression in cultured retinal cells.

11 otocin-induced diabetic rats and in cultured retinal cells.

12 ferating retinal progenitors and postmitotic retinal cells.

13 transport system and NO signaling pathway in retinal cells.

14 e as useful compounds for neuroprotection of retinal cells.

15 ival and proliferation of cultured embryonic retinal cells.

16 lysis comparing human retina to hESC-derived retinal cells.

17 byproducts of the visual cycle accumulate in retinal cells.

18 ellular, and the sera can be internalized by retinal cells.

19 nvolved in hypoxic damage in cultured monkey retinal cells.

20 proliferative capacity of Rb/p107-deficient retinal cells.

21 pically used to characterize the ESC-derived retinal cells.

22 s all the genes present in normal developing retinal cells.

23 with four-way shape entered both corneal and retinal cells.

24 ency of directed differentiation of hESCs to retinal cells.

25 man retinas, downregulated CFH expression in retinal cells.

26 expression of VEGF and TNF-alpha in cultured retinal cells.

27 nes was performed in stem cell-derived human retinal cells.

28 ice grown in aggregates with wild-type mouse retinal cells.

29 organization, with a focus on the retina and retinal cells.

30 e formation and apical displacement of inner retinal cells.

31 s, specifically DARC (Detection of Apoptotic Retinal Cells) [1] and capQ technology [2(**)].

32 In cultured retinal cells, 30-mM glucose exposure increased superoxi

33 The presence of ANT1 in a subset of inner retinal cells accompanied by supernormal ERG responses s

34 is sufficient to retarget neurites of outer retinal cells after ectopic expression.

35 MCP-1 mRNA expression in primarily cultured retinal cells after thermal injury.

36 basic observation that sulindac can protect retinal cells against oxidative stress.

37 ted phosphotyrosine 527 (inhibitory site) in retinal cells, an effect mainly mediated by calcium-perm

38 -dependent attachment of acutely dissociated retinal cells and an L1-expressing, ALCAM-negative cell

39 The morphology of retinal cells and BM were assessed by immunohistochemist

40 kine, IL-27, induced CFH expression in mouse retinal cells and human retinal pigmented epithelial cel

41 We analyzed transcriptomes from 44,808 mouse retinal cells and identified 39 transcriptionally distin

42 that governs the interaction between damaged retinal cells and immune cells to promote tissue repair.

43 ent anti-CMV prodrug that may be taken up by retinal cells and metabolized further to the active anti

44 In retinal cells and mouse retinal tissue, pimonidazole-add

45 ted by the brain during development, whereas retinal cells and stomach parietal cells require normal

46 of the availability of ascorbate to cultured retinal cells and strongly reinforces ascorbate as an im

47 erited blindness have been reprogrammed into retinal cells and successfully transplanted into mice.

48 explore the role of apoptosis of uninfected retinal cells and the contribution of cytokines and othe

49 These substances are highly toxic to retinal cells and the eye has been shown to be unique am

50 eveal a distinct molecular state in dividing retinal cells and their newly postmitotic progeny, and p

51 uronal remodeling of second- and third-order retinal cells and their synaptic terminals in retinas fr

52 ptor and Ras pathway in most differentiating retinal cells, and by both EGF receptor/Ras and by Hedge

53 normally expressed in proliferating central retinal cells, and increased numbers of mitotic cells in

54 e decisions can be made in newly postmitotic retinal cells, and reveal some of the regulators downstr

55 was used to drive overexpression of ngn1 in retinal cells, and siRNA was used to reduce ngn1 express

56 embrane potential and electrical activity of retinal cells, and suggests that K2P channels are well p

57 induces the expression of VEGFA in numerous retinal cells, and that PGC-1alpha expression is strongl

58 IR caused significant retinal cell apoptosis and vascular permeability after 4

59 NT-3 does not affect the well known wave of retinal cell apoptosis that normally occurs during the f

60 As an adhesion molecule, RS1 preserves the retinal cell architecture and promotes visual signal tra

61 The development of stratified retinal cell architecture is highly conserved in all ver

62 esented here are further evidence that inner retinal cells are affected by hyperglycemia simultaneous

63 It is unknown which retinal cells are involved in the retina-to-sclera signa

64 e receptors in certain types of second-order retinal cells are largely desensitized in darkness, lead

65 Furthermore, retinal cells are under constant oxidative stress that c

66 Mouse models with different populations of retinal cells as well as in situ hybridization provided

67 d 96-day human fetal retina and hESC-derived retinal cells at 3 weeks and 9 weeks after induction.

68 vival and function of the highly specialized retinal cells at later stages.

69 Retinal cells become post-mitotic early during post-nata

70 hanges include a five-fold elongation of the retinal cell body and the morphogenesis of the rhabdomer

71 structures smaller than the somas of typical retinal cells can be accessible in living eyes.

72 of (13)C-labeled metabolites, we showed that retinal cells can take up and metabolize (13)C-labeled b

73 Instead, loss of ferroxidases in other retinal cells causes retinal iron accumulation and trans

74 racterized by the progressive destruction of retinal cells, causing the deterioration and eventual lo

75 phogenetic furrow moves and the responses of retinal cells change.

76 molecular atlas of gene expression for known retinal cell classes and novel candidate cell subtypes.

77 In the rodent eye, seven retinal cell classes differentiate in overlapping waves,

78 ontrast to CD4-IRF8KO mice, Irf8 deletion in retinal cells confers protection from uveitis, underscor

79 h) remained in the eye, and up to 70% of the retinal cells contained the nanoparticles.

80 Therefore, embryonic retinal cells could be applied as a cell-based survival

81 etachment (RD) in vivo and in murine primary retinal cell cultures in vitro.

82 n vitro experiments were performed using rat retinal cell cultures incubated in the presence and abse

83 c treatments in whole retina and dissociated retinal cell cultures were used to investigate the cellu

84 ath of retinal ganglion cells in dissociated retinal cell cultures, an effect that was blocked by inh

85 re also evaluated in vitro using dissociated retinal cell cultures.

86 y, we performed comparison analyses of human retinal cell cybrids, which possess identical nuclei, bu

87 However, it had no effect on retinal cell death (TUNEL(+) cells).

88 ongly upregulated, coinciding with increased retinal cell death and expression of proapoptotic protei

89 us exposure of rats to bright light leads to retinal cell death and retinal dysfunction.

90 in marked decreases in hyperglycemia-induced retinal cell death and tumor necrosis factor (TNF)-alpha

91 amage Response 1 (REDD1) in diabetes-induced retinal cell death and visual dysfunction.

92 and a BDNF mimetic are sufficient to rescue retinal cell death and visual function in a vertebrate m

93 Whereas poly(I-C) induced retinal cell death in Rdh8(-/-)Abca4(-/-) and WT mice bo

94 prostacyclin synthase (PGIS) contributes to retinal cell death in vitro and in vivo.

95 Retinal cell death is the main cause of vision loss in m

96 Retinal cell death was analyzed by DNA fragmentation, an

97 After 4 weeks of diabetes, retinal cell death was determined by TUNEL assay.

98 Additionally, AMPA-induced apoptotic retinal cell death was regulated by both NOS and Src act

99 /NO induction may contribute to hypertensive retinal cell death, an increase in mitochondrial OPA1 ma

100 biting apoptosis does not completely prevent retinal cell death, as many enter programmed necrosis or

101 ation of the retina and to prevent apoptotic retinal cell death, which may relate to its proposed rol

102 eins in retinal inflammation that aggravates retinal cell death.

103 modulation is a critical step in excitatory retinal cell death.

104 delayed retinal neurogenesis, and extensive retinal cell death.

105 through which disruptions in NMNAT1 lead to retinal cell degeneration and would provide a resource f

106 months, bugeye mutants exhibit a decrease in retinal cell densities and by 5 months, they show dimini

107 raceable module for automated acquisition of retinal cell density data.

108 rats, 3) insulin-deficient diabetic rats, 4) retinal cells depleted of SOCS6 or overexpressing SOCS1/

109 enes that might regulate specific aspects of retinal cell development, we investigated the expression

110 Research on the basics of how and why retinal cells die in different diseases provides insight

111 nerally considered the main pathway by which retinal cells die in response to a range of noxious stim

112 With more knowledge of how retinal cells die, further advances are being made in pr

113 ze microglial attraction, CSPG induction and retinal cell differentiation.

114 a bZip domain is required for its effects on retinal cell differentiation.

115 ction strategy, we found that Pten regulates retinal cell division and is required to produce the ful

116 (SR) AAV vector administration can transfect retinal cells efficiently, the injection-induced retinal

117 Rb1 leads to the rapid degeneration of most retinal cells except horizontal cells, which persist as

118 the retina of the OIR model and in cultured retinal cells exposed to hypoxia.

119 Cultured retinal cells express a high-affinity ascorbate transpor

120 events during early eye formation determine retinal cell fate and can dictate the behavior of retina

121 The effects of misexpressing NeuroD genes on retinal cell fate determination also suggested shared an

122 It is widely accepted that the process of retinal cell fate determination is under tight transcrip

123 h established mechanisms of early neural and retinal cell fate determination.

124 N-myc is not required for retinal cell fate specification, differentiation, or sur

125 ortance, although their density was altered, retinal cell fates were unaffected.

126 : Stem cells can now be directed to specific retinal cell fates with high yields and acceptable purit

127 ce of retinal progenitor cells for the early retinal cell fates.

128 hown some degree of expression of markers of retinal cells, fewer than 30 markers are typically used

129 y efficient and scalable approach to produce retinal cells for regenerative medicine and for drug-scr

130 Retinal cells from 6 day-old chicken embryos were isolat

131 SOCS1-mediated protection of retinal cells from apoptosis was assessed by annexin V s

132 Mouse embryonic fibroblasts (MEFs) and retinal cells from Csnk1d (CK1delta)-null mice also exhi

133 Embryonic retinal cells from embryonic day (E)7, E10, and E11 prom

134 Dissociated retinal cells from P4 Nrlp-GFP mice were transplanted in

135 53 inactivation but induces reprogramming in retinal cells from reprogrammable mice grown in aggregat

136 The authors also show that SOCS1 protected retinal cells from staurosporine as well as H(2)O(2)-ind

137 Retinal cells from Toxoplasma-infected animals were able

138 to determine whether transplanted embryonic retinal cells from various stages of development influen

139 retina, the impact that this process has on retinal cell function, and how it relates to other patho

140 In cat, most retinal cells have center-surround receptive fields and

141 Also, in normal fibroblasts and retinal cells, hypoxia inhibited the mTOR pathway and su

142 rray and computational analyses of Dicer-CKO retinal cells identified two potential targets of the la

143 ontribute to the establishment of individual retinal cell identity.

144 me non-invasive imaging of single apoptosing retinal cells in animal models of glaucoma and Alzheimer

145 In R28 retinal cells in culture, hyperglycemic conditions enhan

146 amined on how they contribute to the loss of retinal cells in different disease models.

147 generation of superoxide by retina and 661W retinal cells in high glucose and of the alpha1-adrenerg

148 Culturing the retinal cells in high-glucose concentrations enhanced le

149 The ability to resolve single retinal cells in rodents in vivo has applications in rod

150 vidence suggests an important role for outer retinal cells in the pathogenesis of diabetic retinopath

151 her gatifloxacin nor vancomycin was toxic to retinal cells in vitro.

152 VEGF is an important growth factor for many retinal cells, including different types of neurons.

153 se strains with targeted deletion of Irf8 in retinal cells, including microglial cells and a third mo

154 filtrating leukocytes as well as on resident retinal cells, including photoreceptors.

155 Previous studies suggest that a variety of retinal cells, including RPE and Muller glia, may be res

156 er segments (OSs) and increased apoptosis of retinal cells, including those in the outer and inner re

157 As stress in retinal cells increases, phosphorylation of sigmaR1 is i

158 ndogenous products emanating from dying/dead retinal cells induced NF-kappaB and IRF3 activation.

159 aining intrinsically photosensitive ganglion retinal cells (ipRGC) can be assessed by a means of pupi

160 The near transparency of inner retinal cells is advantageous for vision, as light must

161 in Xenopus laevis, whose full complement of retinal cells is formed in 2 days.

162 Their function in retinal cells is just beginning to be elucidated, and a

163 r, the role of Heph and Cp in the individual retinal cells is unclear.

164 aboratory investigation of this multipurpose retinal cell layer.

165 n and other defects, including disruption of retinal cell layers, lack of zymogen granules in the pan

166 etinoschisin supporting interactions between retinal cell layers, so disassembly would prevent struct

167 neration of photoreceptors, but spares other retinal cells, leading to the hope that expression of li

168 ages of different ocular lineages, including retinal cells, lens cells, and ocular-surface ectoderm.

169 etinal degenerations aim to render remaining retinal cells light sensitive once photoreceptors are lo

170 putative promoter, was expressed in a human retinal cell line (ARPE-19) and a Chinese hamster ovary

171 xidant and neuroprotective activity of CA in retinal cell lines exposed to oxidative stress and in a

172 Nrf2 signaling and TP pretreatment protected retinal cell lines from oxidant-induced cell death.

173 al fibrillary acidic protein expression, and retinal cell lines, with YFP-expressing tachyzoites.

174 providing a directional network that ensures retinal cells make the transition from progenitors to ne

175 Retinal cell marker staining showed an orderly array of

176 e eye primordium resulted in loss of Elav, a retinal cell marker; these, however, switched to an Hth-

177 MV-treated Muller cells, their expression of retinal cell markers was compared to that in untreated c

178 elix (bHLH) transcription factors, and other retinal cell markers was tested by double immunohistoche

179 ulation during the early postnatal window of retinal cell maturation and physiological programmed cel

180 Reduction of retinal cell number combined with a loss of the normal c

181 region contains two genes known to modulate retinal cell number.

182 ctivated Kras signaling not only rescued the retinal cell numbers in the Shp2 mutant but also functio

183 hat was accompanied by a similar increase in retinal cell numbers.

184 indicates a regulatory role of eye size for retinal cell numbers.

185 Acutely dissociated retinal cells, obtained from chick embryos, were transpl

186 We showed that the retinal cells of sec13(sq198) failed to form proper nucl

187 produced pronounced GFP expression in inner retinal cells of the fovea, no expression in the central

188 of US on ion channels expressed in neurons, retinal cells, or cardiac cells, which may lead to impor

189 and approaches that could be used to render retinal cells other than atrophied photoreceptors light

190 in retina-specific SOCS1 transgenic rats and retinal cells overexpressing SOCS1/SOCS3.

191 l whereby the Rs1 protein binds to PS in the retinal cell plasma membranes in a calcium-dependent man

192 e retina, and which conjointly identify this retinal cell population in its entirety when using antib

193 logy of any of the non-melanopsin-containing retinal cell populations investigated.

194 HYPOX-4 had no effect on retinal cell proliferation as indicated by BrdU assay an

195 The fact that retinal cell proliferation is elevated after an increase

196 nto the eye, selectively increased tectal or retinal cell proliferation, respectively.

197 the similar organization characterizing the retinal cells providing their input.

198 ssible roles innate immune cells play during retinal cell regeneration, we used intravital microscopy

199 hotoreceptors, followed by progressive inner retinal cell remodeling.

200 ivery of LTA(4) from marrow-derived cells to retinal cells results in the generation of LTB(4) and th

201 analysis of PRDM13 expression in developing retinal cells revealed marked developmental regulation.

202 transcriptomic signatures that lead to each retinal cell's fate determination and development challe

203 In cultured retinal cells, SERPINA3K blocked the overproduction of C

204 Transplanted retinal cells showed poor survival and attracted microgl

205 Retinas were stained with cresyl violet, retinal cell-specific markers, and a human nuclear marke

206 ined with the conserved mammalian pattern of retinal cell specification, this single change in retina

207 tochondrial oxidative stress response within retinal cells, such as prohibitin and MMP2, may serve as

208 ential for photoreceptor differentiation and retinal cell survival in embryonic zebrafish.

209 r, despite a known role for BMP signaling in retinal cell survival, proliferation, and differentiatio

210 n the eye anlage, but only modest effects on retinal cell survival.

211 factor, and insulin, that are essential for retinal cell survival.

212 Our results demonstrated that retinal cell swelling could directly lead to retinal thi

213 o magnetic resonance imaging (MRI) to assess retinal cell swelling in the edematous mouse retina.

214 vasive diffusion MRI was performed to detect retinal cell swelling in vivo.

215 Inner retinal cell swelling was hyperintense on diffusion-weig

216 To assess retinal cell swelling, diffusion MRI was performed at ba

217 The DARC (Detection of Apoptosing Retinal Cells) technology enables in vivo real-time non-

218 e expressed at a higher level in ESC-derived retinal cells than in fetal retina, and most of these we

219 MMF stimulates multiple pathways in retinal cells that potentiate cellular events leading to

220 w that vasopressin is also expressed in many retinal cells that project to the SCN.

221 Progress in retinal-cell therapy derived from human pluripotent stem

222 ugh GCs constitute less than 1% of the total retinal cells, they occur in numerous types and are the

223 ormone prolactin provides trophic support to retinal cells, thus protecting the retina from degenerat

224 photoreceptors among preexisting host outer retinal cells, total photoreceptor layer reconstruction

225 ingle cell profiling of wild-type and N1-CKO retinal cells transitioning from progenitor to different

226 an important component of future therapeutic retinal cell transplantation strategies.

227 s can provide a source of photoreceptors for retinal cell transplantation.

228 roteolysis were significantly reduced in the retinal cells treated with 10 and 100 muM calpain inhibi

229 are characterized by dysfunction of a single retinal cell type and have a high risk of refractive err

230 ription factors leading to the generation of retinal cell type diversity.

231 1 in mature rod photoreceptor cells, another retinal cell type that is severely affected in AMD.

232 oldest syu(+/-) zebrafish, although no other retinal cell type was affected.

233 u(+/-) (syu(+/-)) zebrafish were probed with retinal cell type-specific markers.

234 ulator with physiological functions in every retinal cell type.

235 ntrinsic and extrinsic factors regulate each retinal cell type.

236 thway genes regulate the development of each retinal cell type.

237 and pattern generation from within a single retinal cell type.

238 This tropism suggests that retinal cell-type-specific circuitry sensitizes to Rb lo

239 ned the covariance structure of 12 different retinal cell types across 30 genetically distinct lines

240 specification and differentiation of diverse retinal cell types and subtypes.

241 for the orderly differentiation of the early retinal cell types and whether different bHLH genes have

242 ensional retinal cups that contain all major retinal cell types arranged in their proper layers.

243 Mature retinal cell types expressing PD-1 were identified by im

244 The specification of the seven retinal cell types from a common pool of retina progenit

245 (IGF-I) exerts multiple effects on different retinal cell types in both physiological and pathologica

246 r cloned genes safely and stably to specific retinal cell types in humans.

247 r inhibition influences the behaviors of two retinal cell types known to play roles in pathologic ocu

248 rations of macular xanthophylls (MXs) within retinal cell types manifesting AMD pathology.

249 localization of products from these genes to retinal cell types manifesting AMD-related pathophysiolo

250 Achieving a comprehensive catalog of retinal cell types now appears within reach, because res

251 toreceptor markers were used to detect which retinal cell types were damaged.

252 All retinal cell types were generated throughout nearly the

253 Retinal thickness was measured, retinal cell types were labeled by immunohistochemistry

254 genitors are capable of generating all major retinal cell types, but the RGCs they generate are predo

255 ound defects in the development of all early retinal cell types, including completely failed genesis

256 also contained representation from multiple retinal cell types, including photoreceptors and interne

257 in receptors have been identified in several retinal cell types, including photoreceptors, horizontal

258 ar membrane domains, is expressed in several retinal cell types, including photoreceptors, retinal va

259 l source for regeneration of a wide range of retinal cell types, including retinal ganglion cells and

260 However, no other retinal cell types, including RGCs, were affected in the

261 Two retinal cell types, photoreceptor cells and the adjacent

262 that human blood-derived iPSCs can generate retinal cell types, providing a highly convenient donor

263 As with other retinal cell types, retinal ganglion cells (RGCs) arise

264 Stem cells capable of becoming other retinal cell types, such as photoreceptors, are on the c

265 o examine the roles of myosins in individual retinal cell types, we first used polymerase chain react

266 e essential for the formation of the diverse retinal cell types.

267 lt tissues then differentiated into multiple retinal cell types.

268 nd are manifested distinctively by different retinal cell types.

269 re capable of differentiating into all major retinal cell types.

270 differentiation and maintenance of specific retinal cell types.

271 ase resulted in progressive apoptosis of all retinal cell types.

272 tic cone precursors but not markers of other retinal cell types.

273 vimentin, confirming their presence in both retinal cell types.

274 ining progenitors to produce the rest of the retinal cell types.

275 (RGB) cones in the retina, but not in other retinal cell types.

276 ination and early differentiation of various retinal cell types.

277 ors can give rise to any and all of the main retinal cell types: photoreceptors, interneurons (horizo

278 l barrier caused by apical migration of host retinal cells upon disruption of outer limiting membrane

279 KEY POINTS: Retinal cells use vanilloid transient receptor potential

280 Replacing lost retinal cells via stem cell-based therapies is an exciti

281 TDP-43-NLS accumulation in retinal cells was counteracted by HSP67Bc overexpression

282 The cytosolic fraction of hT17M Rho retinal cells was used to measure the release of cytochr

283 (BrdU) labeling indicated the same number of retinal cells were born in KO and WT mice.

284 Apoptosing retinal cells were counted by 3 masked operators, genera

285 Dissociated monkey retinal cells were cultured for two weeks and subjected

286 Apoptotic retinal cells were identified using the TUNEL technique

287 rthermore, ventral but not dorsal L1(Y1229H) retinal cells were impaired for ephrinB1-stimulated adhe

288 Proliferating retinal cells were labeled by subretinal injection of 5'

289 The cultured retinal cells were physically connected through microcha

290 ly early in the disease process, other inner retinal cells were preserved in the early stages of the

291 The positions of host retinal cells were traced according to their laminar loc

292 Dissociated retinal cells were transferred from green fluorescent pr

293 Cultured retinal cells were treated with CoCl(2) or 2% O(2) to in

294 Cultured retinal cells were used to access the effects of AMPA st

295 shape entered the corneal cells but not the retinal cells, whereas particle with four-way shape ente

296 Transduction of retinal cells with Ad-HSP27 also resulted in photorecept

297 ge after IR, whereas treatment of retinas or retinal cells with Hmgb1 induced a loss of RGCs.

298 Treatment of dissociated retinal cells with siRNA against ngn1 mRNA specifically

299 on of bHLH genes in single, developing mouse retinal cells, with particular emphasis on the NeuroD fa

300 a valuable method of quantifying apoptosing retinal cells, with particular relevance to translation