ライフサイエンスコーパス: Muller

1 Muller cells and macrophages/microglia are likely import

2 Muller cells are principal glial cells in rat retina and

3 Muller cells, unlike neurons, are spread across the reti

4 Muller glia (MG) are the only glial cell type produced b

5 Muller glia (MG) are the principal glial cell type in th

6 Muller glia (MG) function as inducible retinal stem cell

7 Muller glia are capable of de-differentiating and prolif

8 Muller glia can be stimulated to de-differentiate and be

9 Muller glia phagocytose dead photoreceptor cells in a mo

10 Muller glia play diverse, critical roles in retinal home

11 Muller glia, the most abundant glia of vertebrate retina

12 Muller glial cells (MG) generate retinal progenitor (RPC

13 Muller glial cells are the source of retinal regeneratio

14 Muller-McNicoll and colleagues (pp.

15 NAs in adult and young (postnatal day 11/12) Muller glia of the neural retina, we isolated the Muller

16 IL-33(+) Muller cells were more abundant and IL-33 cytokine was e

17 ng their patterns of gene expression, and 5) Muller glia up-regulate specific genes in response to IF

18 f sugar- and amino acid transporters (AATs) (Muller et al., 2015).

19 margins, extended zones of damage, activated Muller cells, microglial recruitment and functional reti

20 emokine and cytokine expression in activated Muller cells.

21 ell-derived cone photoreceptors and an adult Muller glia cell line.

22 RNAs that were not highly expressed in adult Muller glia increased in cultured cells.

23 In freshly isolated adult Muller glia, we identified 7 miRNAs with high expression

24 results thus show the miRNA profile of adult Muller glia and the effects of cell culture on their lev

25 ately before the onset of INM did not affect Muller glia proliferation, but subsequently reduced neur

26 ions of rod bipolar, cone bipolar, amacrine, Muller, and horizontal cells of all cells in the inner n

27 I amacrine cells at postnatal (P) day 5, and Muller glia by P10, when horizontal cells also transient

28 in adult mice and was found in RGC axons and Muller glia, mimicking the MT1-MMP expression pattern se

29 Edn2 has detrimental effects on the BRB and Muller cells that involve interactions with the renin-an

30 ypes and layers including amacrine cells and Muller glia.

31 macrine cells, displaced amacrine cells, and Muller glia were generated between Fd76 and Fd135 along

32 the circumferential marginal zone (CMZ) and Muller glia-derived progenitors have been well described

33 00 mum composed of densely packed cones (and Muller cells) in the central fovea.

34 similarity was found between Ebbinghaus and Muller-Lyer geometrical illusions.

35 lusions, and particularly the Ebbinghaus and Muller-Lyer illusions, correlated with local gray matter

36 ls within the retinal pigment epithelium and Muller cells, but may limit iron transport into the reti

37 lected the topography of AQP4 expression and Muller glial distribution in the human macula.

38 Topography of AQP4 expression and Muller glial distribution were analyzed using Western bl

39 egenerate their retina following injury, and Muller glia (MG) are the source of regenerated neurons.

40 ow that they control bipolar interneuron and Muller glia cell fate specification and promote prolifer

41 d to visualize the response of microglia and Muller glia.

42 radient in the emergence of both neurons and Muller glia with cones, ganglion cells, and horizontal c

43 xia of inner nuclear-layer (INL) neurons and Muller glia.

44 imiting membrane by photoreceptor nuclei and Muller cell microvilli could minimize the light reflecti

45 the subapical regions of photoreceptors and Muller glial cells; rather, it localizes to a small regi

46 DNaseI-seq analysis of the retina and Muller glia shows progressive reduction in accessibility

47 desaturase-1 (DES1), is expressed in RPE and Muller cells.

48 RGR is expressed in human and bovine RPE and Muller glia, whereas mouse RGR is expressed in RPE but n

49 Key to this regenerative response are Muller glia (MG) that respond to injury by reprogramming

50 oposed to accumulate by a mechanism known as Muller's ratchet.

51 lar fitness, similar to the process known as Muller's ratchet.

52 ntifies a subset of bipolar cells as well as Muller glia and astrocytes.

53 amine-fueled anaplerosis that reverses basal Muller cell metabolism from production to consumption of

54 -differentiating and proliferating to become Muller glia-derived progenitor cells (MGPCs) with the ab

55 erved spontaneous cell fusion events between Muller glia and the transplanted cells.

56 OPL and HFL, indicating junctions in between Muller cells and cone axons.

57 We show that targeting both Muller glial cells and photoreceptors with CRB2 ameliora

58 bution of glutamine synthetase, expressed by Muller cells, and zonula occludens-1, a tight-junction p

59 the glucocorticoid receptor are expressed by Muller glia and cells at the retinal margin.

60 growth factor/cytokine that is expressed by Muller glia following neuronal death, is required for Mu

61 roteins, vimentin and GFAP, are expressed by Muller glia, but have different patterns of subcellular

62 oxia, anaplerotic catabolism of glutamine by Muller cells increased ammonium release two-fold.

63 These requirements are partially met by Muller glia and cells of the retinal pigment epithelium

64 glaucoma, upregulates TNFalpha production by Muller cells and microglia.

65 -kappaB pathway are dynamically regulated by Muller glia after neuronal damage or treatment with grow

66 porting a potential mechanism of traction by Muller cells in the CB.

67 del, we show that TNFalpha is upregulated by Muller cells and microglia/macrophages soon after induct

68 Muller cells from diabetic mice with CD40(+) Muller cells.

69 targets were ganglion cells, bipolar cells, Muller cells, and photoreceptors.

70 outer plexiform vascular endothelial cells, Muller glia cells, and the basolateral side of the retin

71 e retinal neurons from intrinsic stem cells, Muller glia, and are a powerful model to understand how

72 We then characterize Muller glia spatial patterning, revealing how individual

73 brane protein present in three cell classes: Muller glia, cone and rod photoreceptors.

74 e type strain for the species, S. coelicolor Muller.

75 Complementary in vitro studies in cultured Muller cells supported these findings and demonstrated t

76 We found primary cultured Muller cells from macula and peripheral retina display s

77 Failing to progress through the cell cycle, Muller glia undergo reactive gliosis, a pathological hal

78 despread Eurasian mayflies, Ephemera danica, Muller 1764 and Serratella ignita (Poda 1761).

79 ns were associated with photoreceptor death, Muller and microglia activation and telangiectasia-like

80 ing the early stage of retinal degeneration, Muller glial cells participated in the phagocytosis of d

81 termine the Young's modulus from a Derjaguin-Muller-Toporov (DMT) fit.

82 t and de Gennes derivation and the Derjaguin-Muller-Toporov model is found.

83 ohnson-Kendall-Roberts theory, the Derjaguin-Muller-Toporov model, adhesive vesicles with surface ten

84 arginal zone, and decreased and disorganized Muller glia.

85 tible mutations, known as Bateson-Dobzhansky-Muller (BDM) incompatibilities, may arise when the two p

86 ents are important candidates for Dobzhansky-Muller hybrid incompatibilities and may contribute to hy

87 We also discovered a two-locus Dobzhansky-Muller hybrid incompatibility.

88 interactions might contribute to Dobzhansky-Muller incompatibilities and be important in speciation.

89 ressing cells (microglia/macrophages) during Muller glia-mediated regeneration, corresponding to a ti

90 l nervous system (CNS) tissue, we eliminated Muller glial cells (MG) from the zebrafish retina.

91 stmortem histologic artifact of eosinophilic Muller cell foot process swelling that mimics a nerve fi

92 iew demonstrates an artifact of eosinophilic Muller cell foot processes swelling in postmortem examin

93 ia in young mice, where the Ascl1-expressing Muller glia give rise to amacrine and bipolar cells and

94 Elimination of TRPC1 facilitated Muller gliosis induced by the elevation of intraocular p

95 Finally, Muller-HSPC hybrids differentiated into photoreceptors.

96 e of the differences between mammal and fish Muller glia that bears on their difference in regenerati

97 viating interference competition (the Fisher-Muller effect) or by separating them from deleterious lo

98 s of K2P channel expression are observed for Muller cells (TWIK-1, TASK-3, TRAAK, and TREK-2) and ret

99 ia following neuronal death, is required for Muller glia to progress through the cell cycle.

100 nced retinal disease highlighting a role for Muller cells and may inform future therapeutic strategie

101 Foveal Muller cells may play an integral role in the transmissi

102 he eukaryote origin that allowed escape from Muller's ratchet--the origin of eukaryotic recombination

103 duced release of inflammatory mediators from Muller cells, inhibited accumulation of mononuclear phag

104 bilities, fish have robust regeneration from Muller glia (MG).

105 encoding both Stim and all known Orai genes; Muller glia predominantly express stromal interacting mo

106 Lactate-stimulated GPR81 Muller cells produce numerous angiogenic factors, includ

107 primary mouse Muller glial cells and a human Muller glia cell line (M10-M1 cells).

108 Our results identify Muller cell CRALBP as a key component of the retinal vis

109 ve microglia influence how NF-kappaB impacts Muller glia reprogramming.

110 In Muller cells, hyperglycemic conditions attenuated global

111 -1alpha in retinal neurons and HIF-2alpha in Muller glia play distinct roles in retinal vascular deve

112 e hybrid retinas and expressed abundantly in Muller cells, is the enzyme that drives this reaction.

113 ne expression and chromatin accessibility in Muller glia from zebrafish, chick, and mice in response

114 ound that Jak/Stat-signaling is activated in Muller glia in response to NMDA-induced retinal damage o

115 form, mTor signaling is rapidly activated in Muller glia.

116 x2 in both early- and late-stage RPCs and in Muller glia.

117 Our studies indicate that CD40 in Muller cells is sufficient to upregulate retinal inflamm

118 cule cluster of differentiation 40 (CD40) in Muller glia has been implicated in the initiation of dia

119 croglia induced secondary gliotic changes in Muller cells, neuronal apoptosis, and decreased light-ev

120 s in the regulation of potassium channels in Muller cells and subsequently in the promotion of glutam

121 c rodents and by hyperglycemic conditions in Muller cells concomitant with increased VEGF expression.

122 s mediated by the 11-cis selective CRALBP in Muller cells.

123 sis entering the tricarboxylic acid cycle in Muller cells accompanied by increased glutamine consumpt

124 lpha (Pdgfralpha)-Cre mice to delete Des1 in Muller cells.

125 TNF-alpha was not detected in Muller cells from diabetic mice with CD40(+) Muller cell

126 and specific expression of exogenous Dp71 in Muller cells leads to correct localization of Dp71 prote

127 that CD40 protein expression is elevated in Muller glia of diabetic mice; however, the mechanisms re

128 Swelling and [Ca(2+)]i elevations evoked in Muller cells by hypotonic stimulation were antagonized b

129 lipase A(2) (PLA(2)) activity exclusively in Muller cells.

130 During diabetes, mice with CD40 expressed in Muller cells upregulated retinal tumor necrosis factor-a

131 ese results indicate that Des1 expression in Muller cells is not required for cone visual pigment reg

132 , we use ShH10 to restore Dp71 expression in Muller cells of Dp71 deficient mouse to study molecular

133 leted in colorectal carcinoma), was found in Muller cells and astrocytes.

134 P = 0.03, Student's t test), and gliosis in Muller cells (at 6 mo, using SPION-glial fibrillary acid

135 ression responses consistent with hypoxia in Muller glia and retinal neurons, and we find a metabolic

136 the putative all-trans retinol isomerase in Muller cells, appears to be 9-cis retinol.

137 in neurons and expressed at lower levels in Muller glia, such as miR-124.

138 CD40 ligation in Muller cells triggered phospholipase C-dependent ATP rel

139 ne cytoskeletal protein, expressed mainly in Muller cells that provide a mechanical link at the Mulle

140 ents via an elegant biochemical mechanism in Muller glial cells of the neural retina that can contrib

141 eas mouse RGR is expressed in RPE but not in Muller glia.

142 nalysis revealed Des1 expression not only in Muller glia but also throughout the retina and in the re

143 ate in part through an additional pathway in Muller cells of the neural retina.

144 ties of store-operated signaling pathways in Muller cells, these studies expand the current knowledge

145 show that GPR81, localized predominantly in Muller cells, governs deep vascular complex formation du

146 aldehyde binding protein (CRALBP) present in Muller cells.

147 eaction to injury is even more pronounced in Muller glia in young mice, where the Ascl1-expressing Mu

148 retinas prevented the accumulation of pS6 in Muller glia and reduced numbers of proliferating MGPCs.

149 amage, insulin, IGF1 and FGF2 induced pS6 in Muller glia, and this was blocked by mTor inhibitor.

150 we show that the store-operated response in Muller cells, radial glia that perform key structural, s

151 not cause TNF-alpha or IL-1beta secretion in Muller cells.

152 MMP-2 expression was seen in Muller glia, predominantly in their end feet, which is i

153 crine cell subtypes but not significantly in Muller cells or photoreceptors.

154 waves reliably induce calcium transients in Muller glial cells (MCs).

155 of 4E-BP1 promotes Cd40 mRNA translation in Muller glia.

156 n the physiological range activated TRPV4 in Muller glia and Xenopus oocytes, but required phospholip

157 ed the CNTF responsive cell types, including Muller glia, rod and cone photoreceptors, and bipolar ce

158 ich maintain and restore quiescence, induces Muller glia to proliferate and generate neurons in adult

159 ompared miRNA expression of acutely isolated Muller glia with those that were maintained in dissociat

160 In this issue, Muller and Nieduszynski find that early replication is a

161 ransition-metal catalysis' by Daniel Janssen-Muller et al., Chem.

162 We have recently shown in this journal (Muller et al.

163 an error in the spelling of the author Jule Muller, which was incorrectly given as Julia Muller.

164 Muller, which was incorrectly given as Julia Muller.

165 verage) do not appear to have any sex-linked Muller F elements (typical for many Diptera) and exhibit

166 In human MIO-M1 Muller cell cultures, REDD1 deletion prevented oxidative

167 Further, macroglial Muller cells, which influence the integrity of the BRB a

168 Macular Muller cells expressed more phosphoglycerate dehydrogena

169 s were increased in primary cultured macular Muller cells which were more susceptible to oxidative st

170 vealed shared molecular mechanisms that make Muller glia attractive targets for cellular reprogrammin

171 Stratified outer nuclear layer with many Muller cells suggests high sensitivity to dim conditions

172 ells, and late-stage progenitors or maturing Muller glia.

173 In healthy retinas of wild-type mice, Muller glial cells phagocytosed cell bodies of dead rod

174 In this issue of Cell Host & Microbe, Muller et al. (2015) show that beta-lactam treatment of

175 n error in the spelling of the author Miryam Muller, which was incorrectly given as Miryam Mueller.

176 Additionally, the mislocalized Muller cells are observed in the photoreceptor layer in

177 photoreceptors, bipolar cells, mitochondria, Muller cells, and retinal pigment epithelium (RPE) cells

178 was performed using the voxel-based modified Muller-Gartner method (PVELab, SPM8).

179 For PVEC, the modified Muller-Gartner method was performed.

180 um entry that replenishes ER stores in mouse Muller cells.

181 oteins to reveal the fine structure of mouse Muller arbors.

182 defines the anatomical arrangement of mouse Muller glia and their network in the radial and tangenti

183 n central carbon metabolism in primary mouse Muller glial cells and a human Muller glia cell line (M1

184 tinal pigment epithelium and for neighboring Muller glial cells.

185 y on P2RX7 caused further neurodegeneration, Muller cell gliosis, progenitor proliferation, and micro

186 Nearly 50% of Muller glia engaged in phagocytosis.

187 knockout (MIFKO) had greater accumulation of Muller glia pERK expression in the detached retina, sugg

188 last wave pressure resulted in activation of Muller glia, loss of photoreceptor cells, and an increas

189 f cone proteins, and decreased activation of Muller glial cells.

190 competent retinal progenitors, activation of Muller-specific gene expression, and terminal differenti

191 n mouse, about the anatomical arrangement of Muller cells and their arbors, and how these features ar

192 A focal artifact of Muller cell foot process swelling was identified in most

193 equence of loss of control with depletion of Muller cells and exposure of the remaining retinal vesse

194 hways that promote the de-differentiation of Muller glia and proliferation of MGPCs.

195 tural change is supported by distribution of Muller cells and patterns of AQP4 expression.

196 n vivo structural and functional evidence of Muller glial dysfunction in eyes of patients with AQP4-I

197 e-like structures along the radial fibers of Muller glia.

198 roles of mTor signaling in the formation of Muller glia-derived progenitor cells (MGPCs) in the chic

199 glia are known to influence the formation of Muller glia-derived progenitor cells (MGPCs), but the me

200 Taken together, the phagocytic function of Muller glia is responsible for retinal homeostasis and r

201 llular reprogramming leading to induction of Muller glia-derived progenitor cells (MGPCs) with stem c

202 ng of retinal neurogenesis and lamination of Muller glia in the mouse retina.

203 MacTel zone that coincides with the loss of Muller cells and macular pigment.

204 e-cell imaging revealed that the majority of Muller glia nuclei migrated to the outer nuclear layer (

205 ith IGF1 stimulated the nuclear migration of Muller glia, but not the formation of MGPCs.

206 We show that the nuclei of Muller glia and NPCs migrate apically and basally in pha

207 crine and bipolar cells, while the number of Muller glia is increased.

208 sents a potential solution to the paradox of Muller's ratchet without loss of function.

209 In addition, abnormal positioning of Muller cell bodies and bipolar cells was evident through

210 The local precision of Muller glia organization suggests that their morphology

211 AQP4 in the end feet and radial processes of Muller astroglia.

212 ion suppressed the improper proliferation of Muller cells and promoted the regression of vascular ves

213 HSPCs enhanced survival and proliferation of Muller-HSPC hybrids as well as their reprogramming into

214 isms controlling the stem cell properties of Muller glia in zebrafish may provide cues to unlock the

215 ledge regarding spontaneous reprogramming of Muller glia in zebrafish and compares this knowledge to

216 ng pathways that drives the reprogramming of Muller glia into MGPCs in the zebrafish retina is the Ja

217 echanisms that suppress the reprogramming of Muller glia into neurogenic progenitors is key to harnes

218 g 'hub' that suppresses the reprogramming of Muller glia into proliferating MGPCs and this 'hub' coor

219 of inflammation, during the reprogramming of Muller glia into proliferating progenitors.

220 ponses most closely resemble the response of Muller glia in the Ndp (KO) retina.

221 , has been linked to a loss in the retina of Muller glial cells and the amino acid serine, synthesize

222 ( Rho(P23H/P23H)), we clarified the roles of Muller glia in the phagocytosis of rod photoreceptor cel

223 We assessed cone functional dependence on Muller cell-expressed Des1 through a conditional knockou

224 enzyme in serine synthesis) than peripheral Muller cells.

225 re more activated in macular than peripheral Muller cells.

226 extracellular space between photoreceptors, Muller glial processes were identified.

227 lacking RDH10 either in cone photoreceptors, Muller cells, or the entire retina.

228 ls: rod photoreceptors, cone photoreceptors, Muller glia, bipolar cells, amacrine cells, retinal gang

229 g the ERG b-wave and oscillatory potentials, Muller cell reactive gliosis, and neuronal cell death, a

230 that regulate the formation of proliferating Muller glia-derived progenitor cells (MGPCs) are beginni

231 (Rock2b) similarly disrupted INM and reduced Muller glial cell cycle reentry.

232 e located in regions containing regenerative Muller glia and are likely engaged in active vesicle tra

233 lar hypertension (COH) in rat down-regulated Muller cells Kir2.1, Kir4.1, TASK-1, GS and GLAST expres

234 ive A2A AR antagonist SCH442416 up-regulated Muller cell Kir4.1, TASK-1, GS and GLAST expressions and

235 tify gene regulatory networks that reprogram Muller glia into progenitor cells, we profiled changes i

236 oreceptors can be generated by reprogramming Muller glia and that this approach may have potential as

237 search efforts directed toward reprogramming Muller glia in mammals.

238 rced expression of Ascl1 in vitro reprograms Muller glia to a neurogenic state.

239 onse mediated by the reentry of the resident Muller glia into the cell cycle.

240 Bergmann glia and retinal Muller cells, nonforebrain astrocytes that have not been

241 or alpha (PPARalpha) is expressed in retinal Muller cells, endothelial cells, and in retinal pigment

242 deletion of Dicer1 (Dicer-CKOMG) in retinal Muller glia (MG).

243 Injury induces retinal Muller glia of certain cold-blooded vertebrates, but not

244 h all glial cells, the major role of retinal Muller glia (MG) is to provide essential neuronal suppor

245 a, neuronal alterations, and loss of retinal Muller glial cells resembling human macular telangiectas

246 inal pigment epithelium (RPE) and/or retinal Muller glia.

247 Here, we demonstrate that retinal Muller glia can be reprogrammed in vivo into retinal pre

248 Chromophore supply by the retinal Muller cells (retina visual cycle) supports the efficien

249 ersely, overexpression of sEH in the retinal Muller glial cells of non-diabetic mice resulted in simi

250 ne-a loss-of-function mutants of both sexes, Muller glia initiate the appropriate reprogramming respo

251 cascades form the basis of a new single-shot Muller matrix polarimeter with potential for endoscopic

252 Since Muller cells synthesize retinal serine, we propose that

253 the slow PII component, suggesting specific Muller cell dysfunction.

254 With cell cycle progression stalled, Muller glia undergo reactive gliosis, a pathological hal

255 s required, but not sufficient, to stimulate Muller glia to give rise to proliferating progenitors, a

256 eneration in the zebrafish retina stimulates Muller glia (MG) to proliferate and generate multipotent

257 In Triassic-Jurassic strata, Muller Canyon, Nevada, Hg levels rise in the extinction

258 han 3 months, demonstrated diffusely swollen Muller cell foot processes with intensely eosinophilic c

259 e experimental diabetic retinopathy and that Muller cells orchestrate inflammatory responses in myelo

260 We further demonstrate that Muller gliogenesis induced by misexpression of the poten

261 Western blotting demonstrated that Muller cell-specific AQP4 was expressed at a higher leve

262 ring cells in different colors, we find that Muller glia tile retinal space with minimal overlap.

263 lamination, which we then used to find that Muller glia, but not RPE cells, are essential for this p

264 Those observations indicated that Muller glial cells are the primary contributor to phagoc

265 explores the nature of the cis retinol that Muller cells in the retina provide to cones for the rege

266 Recent work has revealed that Muller glia are the source of regenerated neurons in zeb

267 sion in the detached retina, suggesting that Muller survival pathways might underlie the neuroprotect

268 Among the Muller phagosomes, >90% matured into phagolysosomes.

269 rn type II cone bipolar cells as well as the Muller glia.

270 cells that provide a mechanical link at the Muller cell membrane by direct binding to actin and a tr

271 n-evoked calcium influx was initiated at the Muller end-foot and apical process, triggering centrifug

272 nd the amino acid serine, synthesized by the Muller cells.

273 ithelium (RPE) and limited expression in the Muller glia.

274 r glia of the neural retina, we isolated the Muller glia from Rlbp-CreER: Stop(f/f)-tdTomato mice by

275 hat RGR opsin is a critical component of the Muller cell visual cycle and that regeneration of cone v

276 bp1 and Glul, and the failure of many of the Muller glia to repress the bipolar/photoreceptor gene Ot

277 nt leads to a reduction in expression of the Muller glia-specific genes Rlbp1 and Glul, and the failu

278 but nonetheless activated expression of the Muller marker P27(Kip1) in Lhx2-deficient cells.

279 The primary glial cells in the retina, the Muller glia, differentiate from retinal progenitors in t

280 Here, we revisit the Muller's ratchet principle applied to the aging of somat

281 We tested the Muller-Lyer, Ebbinghaus, Ponzo, and vertical-horizontal

282 ence between them may be the nature of their Muller cells.

283 ssary for providing neurogenic competence to Muller glia in fish and birds after retinal injury are n

284 sing mice with CD40 expression restricted to Muller cells, we identified a mechanism by which Muller

285 We tested if CRB expression restricted to Muller glial cells or photoreceptors or co-expression in

286 nd vascular pathogenic pathways secondary to Muller cell dysfunction, the cause of which remains obsc

287 on could also make the genome susceptible to Muller's ratchet.

288 iated virus (AAV) variant, ShH10, transduces Muller cells in the Dp71-null mouse retina efficiently a

289 t to accumulation of deleterious alleles via Muller's ratchet.

290 -retinal from the RPE, possibly imported via Muller cells.

291 operculated land snail Cyclophorus volvulus (Muller, 1774) is a good example since it shows a high de

292 pmental window at postnatal Days 6 to 9 when Muller arbors first colonize the synaptic layers beginni

293 if the retinoid cycle was inhibited, or when Muller glia were poisoned.

294 er cells, we identified a mechanism by which Muller cells trigger proinflammatory cytokine expression

295 -characterized retina visual cycle, in which Muller cells recycle spent all-trans-retinol visual chro

296 ganglion cells, but becomes associated with Muller glia and MGPCs following retinal damage.

297 ion also promoted Cd40 mRNA association with Muller cell-specific ribosomes isolated from the retina

298 ofile of cavities around MHs correlates with Muller cell morphology and is consistent with the hypoth

299 dition, zonula occludens-1 co-localized with Muller cells within the complex of OPL and HFL, indicati

300 In the retina of zebrafish, Muller glia have the ability to reprogram into stem cell