ライフサイエンスコーパス: foot process

1 xpression of HMP2 during regeneration of the foot process.

2 nsdifferentiation of basal disk cells of the foot process.

3 rol of dynamics of actin cytoskeleton in the foot processes.

4 where it is required during the formation of foot processes.

5 had normal glomerular morphology and intact foot processes.

6 enal glomerular filtration barrier via their foot processes.

7 pecialized cell junctions that link podocyte foot processes.

8 increased albuminuria and fusion of podocyte foot processes.

9 lar basement membrane and flattened podocyte foot processes.

10 r cell death, and higher density of podocyte foot processes.

11 , which is highly concentrated in astrocytic foot processes.

12 y via a series of interdigitating actin-rich foot processes.

13 rosis, and retraction of glomerular podocyte foot processes.

14 s, where they colocalize with nephrin in the foot processes.

15 lization and failure to form normal podocyte foot processes.

16 rnal limiting membrane, into the Muller cell foot processes.

17 for calcium signaling in their vascular end-foot processes.

18 d the vessels interconnecting astrocytic end-foot processes.

19 ocyte-independent proteinuria with preserved foot processes.

20 and, with VEGF, was concentrated in podocyte foot processes.

21 letal network found in their cell bodies and foot processes.

22 does not prevent effacement of the podocyte foot processes.

23 ibrillary acidic protein (GFAP) on astrocyte foot processes.

24 ane vesicles within podocyte cell bodies and foot processes.

25 merular podocytes were unable to form mature foot processes.

26 l proteins present in high concentrations in foot processes.

27 appearance of TJ-like structures between the foot processes.

28 t and microvillus transformation of podocyte foot processes.

29 an important role for N-WASP in maintaining foot processes.

30 ucleation, is required to stabilize podocyte foot processes.

31 nd strikingly altered morphology of podocyte foot processes.

32 lbuminuria and showed effacement of podocyte foot processes.

33 on their intricate structure, which includes foot processes.

34 ut mice exhibited defects in epithelial cell foot processes, accompanied by mesangial cell hyperplasi

35 the hypothesis that hsp27, by regulating GEC foot process actin polymerization, may be important in m

36 rms are expressed, was enriched in astrocyte foot-processes adjacent to microcapillaries; clusters in

37 ze and quantitate ultrastructural changes to foot processes after podocyte injury.

38 ly protected from effacement of the podocyte foot processes, albuminuria, and glomerulosclerosis.

39 hways are functionally inhibited, glomerular foot process and glomerular basement membrane morphology

40 ng a cooperative role for these molecules in foot process and slit diaphragm formation.

41 aries, effaced podocytes with extremely wide foot processes and albuminuria.

42 ses characterized by loss of interdigitating foot processes and decreased expression of components of

43 ype IV collagen) and associated with widened foot processes and decreased filter efficiency (proteinu

44 ctron microscopy revealed shortened podocyte foot processes and fewer slit diaphragms among the trans

45 ed in maintenance of the architecture of the foot processes and filtration slits characteristic of th

46 between nephrin and other components of the foot processes and filtration slits, especially adherens

47 d by inhibition of the formation of podocyte foot processes and glomerular basement membranes.

48 in retraction of glomerular epithelial cell foot processes and glomerular epithelial cell detachment

49 deletion resulted in coarsening of podocyte foot processes and marked attenuation of Nephrin phospho

50 ion and diffuse effacement of the epithelial foot processes and microvillous transformation of the re

51 rogressive loss of nephrin from the podocyte foot processes and prominent changes in the morphology o

52 ssive disappearance of nephrin from podocyte foot processes and retention of CD2AP.

53 LMX1B regulates the development of podocyte foot processes and slit diaphragms, but studies using po

54 active cell line included fusion of podocyte foot processes and subepithelial and subendothelial depo

55 t reduced levels of proteins associated with foot processes and the glomerular slit diaphragm likely

56 Podocyte foot processes and the interposed glomerular slit diaphr

57 ntain the characteristic architecture of the foot processes and the patency of the filtration slits.

58 reduced podocytes, widespread effacement of foot processes, and modest proteinuria.

59 ar basement membrane, effacement of podocyte foot processes, and reduced sialylation of the major pod

60 tomic features of podocytes down to tertiary foot processes, and we were able to visualize and quanti

61 hat zebrafish crb2b is required for podocyte foot process arborization, slit diaphragm formation, and

62 molecular mechanisms that safeguard podocyte foot process architecture and maintain the three-dimensi

63 ical for glomerular permselectivity; loss of foot process architecture results in proteinuria and FSG

64 gest that in podocytes, PC may also regulate foot process architecture through RhoA.

65 The GEC foot processes are an essential part of the kidney's fil

66 Podocyte cell protrusions (foot processes) are critical for glomerular permselectiv

67 Lmx1b(-/-) podocytes have reduced numbers of foot processes, are dysplastic, and lack typical slit di

68 ssion and localization of slit diaphragm and foot process-associated proteins appeared normal at earl

69 complex expansions resembling interdigitated foot processes at the basal surface.

70 glycan protein complex located in astrocytic foot processes at the blood-brain barrier.

71 d exclusively to lateral margins of podocyte foot processes at the insertion of the slit diaphragm.

72 red thickened and "moth-eaten," and podocyte foot processes became effaced.

73 thelial delamination and widespread podocyte foot process broadening, and glomerular basement membran

74 ic individuals correlated with the extent of foot process broadening.

75 f hydraulic permeability, primarily owing to foot process broadening.

76 the junction between the body column and the foot process, but also as far apically as the base of th

77 lomerular slit diaphragms between epithelial foot processes, but its role in the pathogenesis of this

78 ort GBM thickenings beneath effaced podocyte foot processes, but morphologically normal GBM was signi

79 visualization of single podocytes and their foot processes by conventional fluorescence microscopy.

80 Astrocyte foot processes can signal vascular smooth muscle by arac

81 -treated rats, which show a dramatic loss of foot processes, comparable to that seen in the nephrotic

82 complex was detected in the differentiated, foot process-containing podocytes.

83 gate how regulation of actin dynamics within foot processes controls local morphology.

84 ell apoptosis, delayed and abnormal podocyte foot process development, a complete absence of slit dia

85 ge amounts of GBM laminins, and (3) podocyte foot process differentiation may require direct exposure

86 anization of the slit diaphragm, followed by foot process disappearance, flattening and fusion of maj

87 5%) versus those with mild (</=25%) podocyte foot process effacement (13,030 vs. 4806 pg/mL; P=0.02).

88 The significant degree of foot process effacement (mean 34%, five of 14 cases with

89 damaged the isolated glomeruli, resulting in foot process effacement and albumin leakage.

90 one model of podocyte injury and attenuated foot process effacement and associated proteinuria in a

91 cating altered actinomyosin contractility in foot process effacement and compromised filtration capac

92 Ultrastructural studies revealed podocyte foot process effacement and deposition of extracellular

93 Podocyte foot process effacement and disruption of the slit diaph

94 omerular nodules and causes diffuse podocyte foot process effacement and F-actin collapse via nephrin

95 agi-2-null kidneys revealed diffuse podocyte foot process effacement and focal podocyte hypertrophy b

96 ng albuminuria by 6 weeks and focal podocyte foot process effacement and glomerulosclerosis at 3 mont

97 tophagosomes in the podocytes, with complete foot process effacement and irregular and thickened glom

98 ired recovery from protamine sulfate-induced foot process effacement and lipopolysaccharide-induced n

99 Podocyte foot process effacement and loss of slit diaphragm follo

100 le shortly after birth and preceded podocyte foot process effacement and loss of slit diaphragms by a

101 changes in the epithelium, as they preceded foot process effacement and loss of slit diaphragms.

102 Podocyte dysfunction, represented by foot process effacement and proteinuria, is often the st

103 The mice developed podocyte foot process effacement and proteinuria, which were prev

104 pression, which is a key factor for podocyte foot process effacement and proteinuria.

105 1 resulted in similar phenotypes of podocyte foot process effacement and proteinuria.

106 rin protected mice from LPS-induced podocyte foot process effacement and proteinuria.

107 ponse by activating SFKs and FAK, leading to foot process effacement and proteinuria.

108 ssion was increased, accompanied by podocyte foot process effacement and proteinuria.

109 the common final pathway leading to podocyte foot process effacement and proteinuria.

110 on induced dramatically more albuminuria and foot process effacement and reduced glomerular nephrin m

111 stronger CaMKII activation, reduced podocyte foot process effacement and reduced levels of proteinuri

112 eptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a m

113 pansion of the mesangial matrix and podocyte foot process effacement are attenuated.

114 hese mice were protected from acute podocyte foot process effacement following protamine sulfate perf

115 ure are similar to those used in vivo during foot process effacement in a subset of glomerular diseas

116 SC58236 also reduced Adriamycin-induced foot process effacement in both the COX-2 transgenic mic

117 ctron microscopy revealed prominent podocyte foot process effacement in Daf1(-/-) mice with more wide

118 docyte-specific deletion of Crk1/2 prevented foot process effacement in one model of podocyte injury

119 n could be a final common pathway leading to foot process effacement in proteinuric diseases.

120 was associated with diffuse epithelial cell foot process effacement in the absence of peripheral glo

121 amination of podocytes confirmed more robust foot process effacement in the knockout animals.

122 zebrafish knockdown model and mild podocyte foot process effacement in the mouse model, whereas all

123 omycin aminonucleoside, an agent that causes foot process effacement in vivo, disrupted actin and nep

124 ivation of FAK abrogated the proteinuria and foot process effacement induced by glomerular injury.

125 summary, these data establish that podocyte foot process effacement is a migratory event involving a

126 tand better the mechanisms by which podocyte foot process effacement leads to proteinuria and kidney

127 as-Crk1/2-dependent complex is necessary for foot process effacement observed in distinct subsets of

128 We observed pronounced podocyte foot process effacement on long stretches of the filtrat

129 whether proteinuria is a result of podocyte foot process effacement or the cause of it.

130 Induction of nephrotic syndrome and GEC foot process effacement using the puromycin aminonucleos

131 ificant increase in proteinuria and podocyte foot process effacement with a reduction in the expressi

132 The Cmas(nls) mouse exhibited podocyte foot process effacement, absence of slit diaphragms, and

133 rular filtration barrier integrity, podocyte foot process effacement, and an edematous phenotype.

134 aphs showed collapsed capillaries, extensive foot process effacement, and dysmorphic mitochondria in

135 exhibited early onset albuminuria, podocyte foot process effacement, and elevated systolic BP.

136 ocytes of adult mice results in proteinuria, foot process effacement, and glomerulosclerosis.

137 iculum, resulted in progressive albuminuria, foot process effacement, and histology consistent with E

138 lly in podocytes display severe proteinuria, foot process effacement, and kidney failure.

139 hypertrophy, glomerular basement thickening, foot process effacement, and podocyte loss, resulting in

140 in increased proteinuria, increased podocyte foot process effacement, and to decreased podocyte numbe

141 Electron microscopy revealed an early foot process effacement, as well as morphologic abnormal

142 gene expressors developed heavy proteinuria, foot process effacement, GBM thickening, and renal failu

143 tion of albuminuria, improvement of podocyte foot process effacement, increased glomerular AMPK activ

144 erved in glomeruli of mutant mice, including foot process effacement, irregular and split areas of th

145 n the filtration barrier, including podocyte foot process effacement, irregular thickening of the glo

146 king aspects of human renal disease, such as foot process effacement, mesangial expansion, and glomer

147 Here, we report that, in this model of foot process effacement, nephrin dislocates to the apica

148 on induced significant proteinuria, podocyte foot process effacement, nephrin down-regulation, and ne

149 rked by a loss of synaptopodin, nephrin, and foot process effacement, partly regulated by angiopoieti

150 in both native and grafted kidneys, causing foot process effacement, proteinuria and FSGS-like glome

151 onclusion, FAK activation regulates podocyte foot process effacement, suggesting that pharmacologic i

152 lbuminuric mice revealed widespread podocyte foot process effacement, thickening of the glomerular ba

153 SGS, including mesangial sclerosis, podocyte foot process effacement, tubular atrophy, interstitial f

154 Podocytes showed foot process effacement, vacuolar degeneration, detachme

155 nephrotic patients demonstrated at least 80% foot process effacement, whereas no biopsy from a nonnep

156 lomerular basement membrane (GBM) charge and foot process effacement, whereas transgenic expression s

157 and simplification of the cell shape, called foot process effacement, which is a classic feature of p

158 Podocytes showed focal foot process effacement, which was the most likely cause

159 ding basement membrane reaction and podocyte foot process effacement.

160 elial immune deposits and extensive podocyte foot process effacement.

161 of podocyte FAK, followed by proteinuria and foot process effacement.

162 uced injury, with attenuated albuminuria and foot process effacement.

163 laminations and splitting including podocyte foot process effacement.

164 ened glomerular basement membrane, and focal foot process effacement.

165 endothelium can lead to proteinuria without foot process effacement.

166 proteinuria can be observed without podocyte foot process effacement.

167 ted in Lamb2-/- mice, even before widespread foot process effacement.

168 ease most often are associated with podocyte foot process effacement.

169 ion barrier development, leading to podocyte foot process effacement.

170 in vivo, shedding new light on mechanisms in foot process effacement.

171 einuria was diffuse visceral epithelial cell foot process effacement.

172 dramatic change in cell morphology known as foot process effacement.

173 th loss of nephrin-Nck1/2 association during foot process effacement.

174 l changes of the filtration slits resembling foot process effacement.

175 cterized by proteinuria and partial podocyte foot process effacement.

176 otype, resulting in proteinuria and podocyte foot process effacement.

177 ly reduced talin1 cleavage, albuminuria, and foot process effacement.

178 cytes may be responsible for proteinuria and foot process effacement.

179 e mice developed spontaneous proteinuria and foot process effacement.

180 ytes exhibited substantial vacuolization and foot process effacement.

181 ce resulted in proteinuria with only minimal foot process effacement.

182 glomerular basement membrane thickening and foot process effacement.

183 eNOS-deficient sFlt-1 mice exhibited severe foot process effacement.

184 ic lesions of focal glomerular sclerosis and foot process effacement; however, its etiology and patho

185 onal (albuminuria and azotemia), structural (foot-process effacement and glomerulosclerosis) and mole

186 mesonephroi of adult zebrafish, resulting in foot-process effacement and podocyte loss.

187 ic examination shows focal areas of podocyte foot-process effacement in young mice, and diffuse effac

188 (pro)renin receptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion.

189 Transgenic mice also manifested significant foot-process effacement, moderate mesangial expansion, a

190 membrane from the pulling apart of podocyte foot processes, followed by adhesions to the Bowman caps

191 The foot processes form a highly organized structure, the di

192 severe proteinuria due to abnormal podocyte foot process formation.

193 tly reduced the podocyte-matrix adhesion and foot process formation.

194 depends on the normal structure of podocyte foot processes forming a functioning slit diaphragm in b

195 Loss of their foot process (FP) architecture (FP effacement) results i

196 very from protamine sulfate-induced podocyte foot process (FP) effacement and LPS-induced nephrotic s

197 We hypothesized that the degree of podocyte foot process (FP) effacement in postreperfusion transpla

198 Electron microscopy demonstrated focal foot process fusion and mesangiolysis.

199 tion, whereas mesangial cell injury leads to foot process fusion and proteinuria.

200 d to attenuate the resulting albuminuria and foot process fusion.

201 normal levels despite severe proteinuria and foot process fusion; no cell proliferation was observed.

202 a mechanism associated to a reduction in the foot-process fusion and desmin, and a recovery of synapt

203 rular basement membrane thickening, podocyte foot-process fusion, and transforming growth factor-beta

204 AQP4, found in astrocyte foot processes, glia limitans and ependyma, facilitates

205 filtration apparatus consisting of podocyte foot processes, glomerular basement membrane and endothe

206 a2alpha1(IV) in GBMs, effacement of podocyte foot processes, gradual loss of glomerular barrier prope

207 the junction between the body column and the foot process, immunofluorescence studies indicated that

208 pithelial GBM thickening but intact podocyte foot processes in aged rescued mice.

209 esses that connect the primary processes and foot processes in Alport mice.

210 ent and swelling of pericapillary astrocytic foot processes in AQP4-deficient mice were significantly

211 Podocyte foot processes in microalbuminuric participants were not

212 odocytes and revealed effacement of podocyte foot processes in Neph1(-/-) mice.

213 ndrial degeneration, mitophagy, and deformed foot processes in podocytes.

214 ially localized to podocyte mitochondria and foot processes in rat kidneys and cultured human podocyt

215 open filtration pathway between neighboring foot processes in the glomerular epithelium by charge re

216 induced oxidative stress, fusion of podocyte foot processes in the kidney glomerulus, and urinary alb

217 -4 (AQP4) water channel located on astrocyte foot processes in the perivessel and subpial areas of th

218 acquire light microscopic images of podocyte foot processes in unprecedented detail, even in living p

219 ere were blunting and widening of the minor (foot) processes in association with altered distribution

220 ic conditions associated with changes in GEC foot processes, indicating their importance for maintain

221 ecifically bind to murine THSD7A on podocyte foot processes, induce proteinuria, and initiate a histo

222 the membrane that might interact across the foot process intercellular junction through interactions

223 the highly complex interdigitating podocyte foot processes is critical to form the normal glomerular

224 GBM residing beneath differentiated podocyte foot processes is inherently and abnormally permeable, a

225 The morphology of healthy podocyte foot processes is necessary for maintaining the characte

226 iform podocyte effacement, very few and wide foot processes joined by occluding junctions, almost com

227 ergo glomerular morphogenesis or express the foot process junctional markers nephrin and podocin.

228 docytes failed to form the normal network of foot processes, leading to defective glomerular maturati

229 ation barrier lead to effacement of podocyte foot processes, leakage of albumin, and the development

230 cell plasma membranes, including glial cell foot processes lining the blood-brain barrier.

231 stored the normal ultrastructure of podocyte foot processes, lowered proteinuria, lowered collagen IV

232 Kidney podocytes and their foot processes maintain the ultrafiltration barrier and

233 ocytes to confirm dynamin's role in podocyte foot process maintenance.

234 copy, that podocin localizes to the podocyte foot process membrane, at the insertion site of the slit

235 otein nephrin results in failure of podocyte foot process morphogenesis and concomitant proteinuria f

236 event nephrin-dependent actin remodeling and foot process morphological changes.

237 which may be important in the regulation of foot process morphology and response to podocyte injury.

238 tant mouse induced a broadened and flattened foot process morphology that was distinct from that obse

239 aotic spatial patterns that could impair the foot process morphology.

240 found a corresponding reduction in podocyte foot process number.

241 ized by structural changes in the actin-rich foot processes of glomerular podocytes.

242 The actin-based foot processes of kidney podocytes and the interposed sl

243 been shown previously to be expressed on the foot processes of podocytes in the kidney glomerulus as

244 regulatory light chain increased in podocyte foot processes of Rhpn1(-/-) mice, implicating altered a

245 alized junctions between the interdigitating foot processes of the glomerular epithelium (podocytes)

246 ge is retraction (effacement) of the distal "foot" processes of glomerular epithelial cells (GEC) whi

247 These observations identify astrocytic end-foot processes plastered at the vessel wall as a center

248 glomerular epithelial cells with established foot processes (podocytes) on the outside.

249 specifically required for the maintenance of foot processes, presumably sustaining the mechanical res

250 est that Ubr4 is a key regulator of podocyte foot process proteostasis.

251 ted P-glycoprotein localization on astrocyte foot process remnants at the abluminal face of the brain

252 l renal diseases characterized by pathologic foot process remodeling, prompting the hypothesis that p

253 changes include formation of interdigitating foot processes, replacement of tight junctions with slit

254 Visualizing podocyte foot processes requires electron microscopy, a technique

255 preserving the normal structure of podocyte foot processes, slit diaphragms, and actin cytoskeleton.

256 rier function results when podocytes undergo foot process spreading and retraction by remodeling thei

257 In the NTS model, we observed a lack of foot process spreading in mouse podocytes with Shp2 dele

258 rat model of podocyte injury at a time when foot process spreading is initially observed.

259 months of age, although they did not exhibit foot process spreading until 8 months, when the rate of

260 Mouse podocytes lacking Shp2 do not develop foot process spreading when subjected to podocyte injury

261 ignaling events are necessary for changes in foot process structure and function following injury.

262 podocyte actin cytoskeleton, regulating the foot process structure and glomerular filter integrity.

263 tion, may be important in maintaining normal foot process structure, and regulating pathophysiologic

264 d slit-diaphragms that form between podocyte foot processes surrounding glomerular blood vessels.

265 Meningitis produced marked astrocyte foot process swelling in wild type but not AQP4 null mic

266 tologic artifact of eosinophilic Muller cell foot process swelling that mimics a nerve fiber layer he

267 A focal artifact of Muller cell foot process swelling was identified in most patients (1

268 ates an artifact of eosinophilic Muller cell foot processes swelling in postmortem examination of you

269 helial cells and neuropil, swollen astrocyte foot processes, swollen and degenerating capillary endot

270 are adjacent to those endoderm cells of the foot process that express high levels of HMMP mRNA.

271 ton regulatory protein expressed in podocyte foot processes that regulates the dynamics of actin fila

272 function depends on fingerlike projections (foot processes) that interdigitate with those from neigh

273 at contributes to the morphology of podocyte foot processes through signaling to the underlying actin

274 ue that allows for visualization of podocyte foot processes using confocal laser scanning microscopy.

275 Broadening of podocyte foot processes was associated with a reduction in the nu

276 density of open slit pores between podocyte foot processes was decreased in db/db diabetes but was p

277 hybrids showed vascularization, but podocyte foot processes were absent.

278 embrane thickness was increased and podocyte foot processes were broadened.

279 teins associated with the slit diaphragm and foot processes were normal, and there were no obvious ul

280 Pericyte foot processes were tightly positioned adjacent to endot

281 ic cell compartments such as kidney podocyte foot processes, where it promotes RhoA signalling by blo

282 ue 3D structure of major and interdigitating foot processes which is the prerequisite for renal blood

283 Movement and retraction of podocyte foot processes, which accompany podocyte injury, suggest

284 GBM width and mesangial foot process width (FPW(mes)) also correlated with prote

285 luorescence microscopy to visualize podocyte foot processes will complement electron microscopy and f

286 as well as extensive effacement of podocyte foot processes with abnormal junctional complexes.

287 d epithelial cells that form interdigitating foot processes with bridging slit diaphragms (SDs) that

288 , demonstrated diffusely swollen Muller cell foot processes with intensely eosinophilic cytoplasm tha

289 lar basement membrane (GBM) and the podocyte foot processes with their modified adherens junctions kn