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

4 e formation and apical displacement of inner retinal cells.

5 is required for ER homeostasis in Drosophila retinal cells.

6 ved to reflect the activities of local outer retinal cells.

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

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

9 modulated autophagosome formation in ARPE19 retinal cells.

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

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

12 wn-regulate PPARalpha expression in cultured retinal cells.

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

14 ferating retinal progenitors and postmitotic retinal cells.

15 transport system and NO signaling pathway in retinal cells.

16 e as useful compounds for neuroprotection of retinal cells.

17 ival and proliferation of cultured embryonic retinal cells.

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

19 byproducts of the visual cycle accumulate in retinal cells.

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

21 nvolved in hypoxic damage in cultured monkey retinal cells.

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

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

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

25 ency of directed differentiation of hESCs to retinal cells.

26 man retinas, downregulated CFH expression in retinal cells.

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

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

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

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

31 protein is expressed at some level in mutant retinal cells.

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

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

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

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

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

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

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

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

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

41 of techniques such as Detection of Apoptotic Retinal Cells and Adaptive Optics confocal Scanning Lase

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

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

44 Retinal cells and genes must be functionally adjusted to

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

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

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

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

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

50 vel, we studied the gene regulation of total retinal cells and retinal endothelial cells during non-i

51 Total retinal cells and retinal endothelial cells from naive a

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

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

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

55 eristic extracellular deposits between outer retinal cells and their blood supply.

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

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

58 se they make more synapses with second-order retinal cells and thus must extrude more Ca(2+) In dayli

59 and fluorescence imaging conducted in murine retinal cells and Xenopus oocytes indicated that cell sw

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 owever, patient-derived organoids maintained retinal cell cytoarchitecture despite significantly redu

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

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

92 nge of diseases characterized by progressive retinal cell death and gradual loss of vision.

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

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

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

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

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

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

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

100 Retinal cell death was analyzed by DNA fragmentation, an

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

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

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

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

105 eins in retinal inflammation that aggravates retinal cell death.

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

107 delayed retinal neurogenesis, and extensive retinal cell death.

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

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

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

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

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

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

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

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

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

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

118 an earlier stage, accumulate within Sac1(ts) retinal cells due to impaired endo-lysosomal degradation

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

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

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

122 Cultured retinal cells express a high-affinity ascorbate transpor

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

124 neuroectodermal/ectodermal fates, including retinal cell fate.

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 roplet (LD)-mediated mechanism of protecting retinal cells from age-related degeneration.

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

144 In R28 retinal cells in culture, hyperglycemic conditions enhan

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

146 PDE6 and, as a consequence, degeneration of retinal cells in eye diseases linked to inflammation and

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

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

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

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

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

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

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

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

157 electrodes designed to leverage migration of retinal cells into voids in the subretinal space.

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

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

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

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

162 Using single-cell RNA sequencing of retinal cells isolated from C57BL/6J mice, we demonstrat

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

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

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

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

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

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

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

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

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

172 Identifying disease-specific patterns of retinal cell loss in pathological conditions has been hi

173 RNA-Seq analysis of total retinal cells mainly brought to light upregulation of ge

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

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

176 MiRNAs are essential for the retinal cell maturation and function; the miR-183 cluste

177 We demonstrate that inner retinal cells migrate into the 25 mum deep honeycomb wel

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

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

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

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

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

183 In parallel, VEGF produced by mixed retinal cells or by mesenchymal stem cells exerted a par

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

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

186 Roughest and Kirre, which coordinate apical retinal cell patterning at an earlier stage, accumulate

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

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

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

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

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

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

193 In differentiating retinal cells, Rbfox2 expression was observed as early a

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

195 hotoreceptors, followed by progressive inner retinal cell remodeling.

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

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

198 ll populations representing all known neural retinal cells: rod photoreceptors, cone photoreceptors,

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

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

201 Transplanted retinal cells showed poor survival and attracted microgl

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

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

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

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

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

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

208 Inner retinal cell swelling was hyperintense on diffusion-weig

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

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

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

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

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

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

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

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

217 cells allow differentiating and mature human retinal cells to be studied in unprecedented detail.

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

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

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

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

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

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

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

225 1 in mature rod photoreceptor cells, another retinal cell type that is severely affected in AMD.

226 ulator with physiological functions in every retinal cell type.

227 ntrinsic and extrinsic factors regulate each retinal cell type.

228 cification and differentiation of each major retinal cell type.

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

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

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

232 as found to be distinct in vivo in different retinal cell types and at different stages.

233 ns that informed the sequential emergence of retinal cell types and enabled identification of stage-s

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

235 All major retinal cell types are observed and marker genes for eac

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

237 egrating more than seven different essential retinal cell types derived from hiPSCs.

238 as progenitor cells produce the 7 classes of retinal cell types during development.

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

240 However, dysfunction of other retinal cell types has also been described, sometimes le

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

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

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

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

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

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

247 A complete molecular atlas of retinal cell types provides an important foundation for

248 /-) retinal phenotype, 4) all major resident retinal cell types respond to interferon gamma (IFNG) by

249 No other retinal cell types were affected by GDF-11 knockout, but

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

251 All retinal cell types were generated throughout nearly the

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

253 etwork-based analysis, we identify all major retinal cell types, and their corresponding gene express

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 ide the MacTel zone that were present in all retinal cell types.

266 uration and specification of all seven major retinal cell types.

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

268 lt tissues then differentiated into multiple retinal cell types.

269 nd are manifested distinctively by different retinal cell types.

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

271 expression observed in directly neighboring retinal cell types.

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

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

274 oward the transcriptomes of adult peripheral retinal cell types.

275 differentiation and maintenance of specific retinal cell types.

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

277 ination and early differentiation of various retinal cell types.

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

279 ular injury or retinal detachment, misplaced retinal cells undergo epithelial to mesenchymal transiti

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

281 We conclude that retinal cells use a cohort of TFs with different express

282 KEY POINTS: Retinal cells use vanilloid transient receptor potential

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

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

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

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

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

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

289 The cultured retinal cells were physically connected through microcha

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

291 Dissociated retinal cells were transferred from green fluorescent pr

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

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

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

295 into the transcriptional landscape of human retinal cells, which is fundamental to understanding ret

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