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

4 ucleation, is required to stabilize podocyte foot processes.

5 nd strikingly altered morphology of podocyte foot processes.

6 lbuminuria and showed effacement of podocyte foot processes.

7 on their intricate structure, which includes foot processes.

8 ional complexes between abnormally broadened foot processes.

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

10 had normal glomerular morphology and intact foot processes.

11 enal glomerular filtration barrier via their foot processes.

12 pecialized cell junctions that link podocyte foot processes.

13 increased albuminuria and fusion of podocyte foot processes.

14 lar basement membrane and flattened podocyte foot processes.

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

16 , which is highly concentrated in astrocytic foot processes.

17 dney's formation of capillary loops abutting foot processes.

18 rosis, and retraction of glomerular podocyte foot processes.

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

20 lization and failure to form normal podocyte foot processes.

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

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

23 d the vessels interconnecting astrocytic end-foot processes.

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

25 ocyte-independent proteinuria with preserved foot processes.

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

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

28 does not prevent effacement of the podocyte foot processes.

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

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

31 t and microvillus transformation of podocyte foot processes.

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

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

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

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

36 Podocyte foot process and slit diaphragm are the final barrier to

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 Podocyte foot processes and the interposed glomerular slit diaphr

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

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

56 t of suPAR on podocyte injury, effacement of foot processes, and proteinuria.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 Astrocyte foot processes can signal vascular smooth muscle by arac

77 THSD7A localizes to the basal aspect of foot processes, closely following the meanders of the sl

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

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

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

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

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

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

84 5%) versus those with mild (</=25%) podocyte foot process effacement (13,030 vs. 4806 pg/mL; P=0.02).

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

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

87 but mitigated hypertension-induced podocyte foot process effacement and albuminuria.

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

89 sis reveals that Robo2 cKO mice display less foot process effacement and better-preserved slit-diaphr

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

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

92 Podocyte foot process effacement and disruption of the slit diaph

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

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

95 while podocytes were edematous with areas of foot process effacement and glomerular basement membrane

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 uria around postnatal day 28, accompanied by foot process effacement and loss of slit diaphragms.

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

103 Patients in a cluster with more prominent foot process effacement and microvillous transformation

104 docytes of the knockout mice had distinctive foot process effacement and microvillus formation.

105 ant insights into the mechanisms of podocyte foot process effacement and points out a promising strat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 serum proteins leak into urine, and podocyte foot process effacement is the common pathway of all pro

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

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

133 Additionally, we observed severe podocyte foot process effacement of remaining podocytes, activati

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

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

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

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

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

139 es alphavbeta3 integrin on podocytes, causes foot process effacement, and contributes to proteinuric

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

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

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

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

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

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

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

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

148 anges were associated with profound podocyte foot process effacement, cell death, and sustained p38 a

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

150 ion is sufficient and necessary for podocyte foot process effacement, however, Rac1 inhibition is not

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

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

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

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

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

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

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

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

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

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

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

162 Podocytes showed foot process effacement, vacuolar degeneration, detachme

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

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

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

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

167 ytes exhibited substantial vacuolization and foot process effacement.

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

169 glomerular basement membrane thickening and foot process effacement.

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

171 ding basement membrane reaction and podocyte foot process effacement.

172 elial immune deposits and extensive podocyte foot process effacement.

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

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

175 laminations and splitting including podocyte foot process effacement.

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

177 ular dysfunction, loss of stress fibers, and foot process effacement.

178 endothelium can lead to proteinuria without foot process effacement.

179 proteinuria can be observed without podocyte foot process effacement.

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

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

182 einuria was diffuse visceral epithelial cell foot process effacement.

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

184 n microcopy analyses showed a focal podocyte foot process effacement.

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

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

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

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

189 cterized by proteinuria and partial podocyte foot process effacement.

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

191 m3 knockdown led to albuminuria and podocyte foot process effacement.

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

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

194 e mice developed spontaneous proteinuria and foot process effacement.

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

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

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

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

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

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

201 in the lower quarter of the taste bud and a foot process extending to the basement membrane often co

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

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

204 severe proteinuria due to abnormal podocyte foot process formation.

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

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

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

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

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

210 Electron microscopy demonstrated focal foot process fusion and mesangiolysis.

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

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

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

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

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

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

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

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

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

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

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

222 Podocyte foot processes in microalbuminuric participants were not

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

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

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

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

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

228 -4 (AQP4) water channel located on astrocyte foot processes in the perivessel and subpial areas of th

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

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

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

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

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

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

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

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

237 rminal region normally localizes to podocyte foot processes, it does not do so in the presence of FSG

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 found a corresponding reduction in podocyte foot process number.

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

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

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

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

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

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

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

260 findings suggest that THSD7A functions as a foot process protein involved in the stabilization of th

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

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

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

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

265 Visualizing podocyte foot processes requires electron microscopy, a technique

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

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

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

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

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

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

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

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

274 ancing podocyte adhesion that helps maintain foot process structure.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

289 Pericyte foot processes were tightly positioned adjacent to endot

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

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

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

293 e injury and loss, as evidenced by increased foot process width (a generally accepted structural mark

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

295 (increasing podocyte GL3 volume fraction and foot process width) was also associated with increasing

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

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

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

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

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