ライフサイエンスコーパス: glomerular basement membrane

1 ion, mesangiosclerosis, and expansion of the glomerular basement membrane.

2 o maintain the structure and function of the glomerular basement membrane.

3 esult of defective type IV collagen in their glomerular basement membrane.

4 s present at birth, despite a grossly normal glomerular basement membrane.

5 the interaction between the podocyte and the glomerular basement membrane.

6 ocytopathy and/or segmental splitting of the glomerular basement membrane.

7 tron-dense deposits and complement C3 on the glomerular basement membrane.

8 tion of type IV collagen alpha3 chain in the glomerular basement membrane.

9 myotendinous junctions, and in kidney to the glomerular basement membrane.

10 ous NC1 domain of alpha3(IV) collagen in the glomerular basement membrane.

11 ith rabbit IgG followed by rabbit anti-mouse glomerular basement membrane.

12 angial matrix expansion or thickening of the glomerular basement membrane.

13 5 depletion nor accumulation of C3 along the glomerular basement membrane.

14 ter the contacts between these cells and the glomerular basement membrane.

15 at proteases are involved in damaging Alport glomerular basement membrane.

16 a exchange in disease induced by antibody to glomerular basement membrane.

17 a number of basement membranes including the glomerular basement membrane.

18 omes (group I) or DNA (group II) adherent to glomerular basement membrane.

19 rular epithelial cells (podocytes) along the glomerular basement membrane.

20 oding type IV collagen chains present in the glomerular basement membrane.

21 on was induced using an antibody against the glomerular basement membrane.

22 ogressive accumulation of laminin 211 in the glomerular basement membrane.

23 ded for normal formation and function of the glomerular basement membrane.

24 l expansion, and segmental thickening of the glomerular basement membrane.

25 ltration barrier on the vascular side of the glomerular basement membrane.

26 ubclass, along the epithelial surface of the glomerular-basement membrane.

27 the formation of podocyte foot processes and glomerular basement membranes.

28 ular matrix deposition, and thickness of the glomerular basement membranes.

29 f serum C3 levels and clearance of iC3b from glomerular basement membranes.

30 ocess effacement and irregular and thickened glomerular basement membranes.

31 ence of the limited fraction of space in the glomerular basement membrane (a concentrated gel) into w

32 Similar glomerular basement membrane abnormalities could offer a

33 merulonephritis induced by heterologous anti-glomerular basement membrane Abs in wild-type (IL-4+/+)

34 ated by binding of heterologous (sheep) anti-glomerular basement membrane Abs to the glomeruli of mic

35 Trinitrophenol was planted on the glomerular basement membrane after conjugation to nephro

36 tric studies of kidneys revealed a thickened glomerular basement membrane and effaced podocytes in th

37 ratus consisting of podocyte foot processes, glomerular basement membrane and endothelial cells.

38 ease, including a thickened and disorganized glomerular basement membrane and flattened podocyte foot

39 Greater width of the glomerular basement membrane and higher levels of glycat

40 rular cells alter cell interactions with the glomerular basement membrane and lead to increased glome

41 experimental glomerulonephritis, being anti-glomerular basement membrane and lipopolysaccharide-indu

42 ith a decreased distribution of VEGFA in the glomerular basement membrane and on endothelial cells.

43 VEGF-A165 b rescues the increase in glomerular basement membrane and podocyte slit width, as

44 es them an attractive experimental model for glomerular basement membrane and possibly other extracel

45 on of extracellular matrix proteins into the glomerular basement membrane and renal mesangial cell hy

46 ention of native ferritin [corrected] in the glomerular basement membrane and systemic blood pressure

47 exogenous CFH ameliorates C3 staining of the glomerular basement membrane and triggers the appearance

48 cterized by progressive deterioration of the glomerular basement membrane and usually associated with

49 arietal epithelial cells attached to denuded glomerular basement membrane and, occasionally, disengag

50 albumin excretion, approximately 3x thicker glomerular basement membranes and severe podocyte efface

51 y was observed only outside laminin-positive glomerular basement membrane, and co-localized with neph

52 cess effacement, irregular thickening of the glomerular basement membrane, and dilated capillary loop

53 an injured endothelial morphology, thickened glomerular basement membrane, and focal foot process eff

54 e foot process effacement, thickening of the glomerular basement membrane, and FSGS-like lesions.

55 ey glomeruli was consistent with that of the glomerular basement membrane, and staining was markedly

56 is comprised of the endothelial lining, the glomerular basement membrane, and the podocyte intercell

57 ac1 also led to podocyte detachment from the glomerular basement membrane, and we detected detached p

58 ters, Ab and complement deposition along the glomerular basement membranes, and a nephrotic syndrome,

59 of HB-EGF in rat kidneys treated with anti- glomerular basement membrane (anti-GBM) antibody (Ab) to

60 Urine samples from mice with anti-glomerular basement membrane (anti-GBM) antibody-induced

61 The pathophysiology of anti-glomerular basement membrane (anti-GBM) disease before c

62 st recruitment in renal fibrosis due to anti-glomerular basement membrane (anti-GBM) disease is unkno

63 r kidneys as a result of posttransplant anti-glomerular basement membrane (anti-GBM) disease.

64 syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and

65 inct, separate disease process, such as anti-glomerular basement membrane antibodies or anti-neutroph

66 racterized by circulating and deposited anti-glomerular basement membrane antibodies, focal necrotizi

67 as been known to occur with exposure to anti-glomerular basement membrane antibody (AGBM-Ab) in the r

68 days later by injection of sheep anti-mouse glomerular basement membrane antibody and CRP or control

69 Injection of sheep anti-glomerular basement membrane antibody into preimmunized

70 In GEC(HO-1) rats with anti-glomerular basement membrane antibody mediated, compleme

71 g parameters both at baseline and after anti-glomerular basement membrane antibody treatment: blood p

72 ered GN with a subnephritogenic dose of anti-glomerular basement membrane antibody, Aire(-/-) mice ha

73 ution of NETs via DNase I did not alter anti-glomerular basement membrane antibody-induced glomerular

74 dulates iNOS expression and activity in anti-glomerular basement membrane antibody-mediated glomerulo

75 unizing mice with MPO and a low dose of anti-glomerular basement membrane antibody.

76 hritis induced by the administration of anti-glomerular basement membrane antibody.

77 re processed for matrix antigen (collagen I, glomerular basement membrane antigens, laminin, and fibr

78 Introduction of heterologous anti-glomerular basement membrane antiserum (nephrotoxic seru

79 uced with a previously described rabbit anti-glomerular basement membrane antiserum nephritis approac

80 The glomerular basement membrane appeared to be thickened an

81 sociation and distribution of SAP within the glomerular basement membrane are altered or completely d

82 The glomerular epithelial cells and the glomerular basement membrane are important constituents

83 ing complexes to dissociate and traverse the glomerular-basement membrane) are compatible with a path

84 s inhibitor prevents focal thickening of the glomerular basement membrane, but does not prevent effac

85 haracterized by accumulation of C3 along the glomerular basement membrane, but the role of properdin

86 gh glucose (HG) in cultured podocytes alters glomerular basement membrane by activating signal transd

87 alpha 3 alpha 4 alpha 5(IV) collagen in the glomerular basement membrane causes Alport syndrome, a h

88 ibodies to type IV collagen that bind to the glomerular basement membrane, causing rapidly progressin

89 inin and type IV collagen composition of the glomerular basement membrane changes during glomerular d

90 increased albuminuria and thickening of the glomerular basement membrane compared with nondiabetic F

91 of podocytes and had better integrity of the glomerular basement membrane compared with untreated Col

92 laminin alpha5 (Lama5), a major tubular and glomerular basement membrane component that is important

93 -linked hereditary nephropathy (XLHN) have a glomerular basement membrane defect that leads to progre

94 Several glomerular basement membrane defects include Alport's sy

95 crosis by light microscopy or electron-dense glomerular basement membrane deposits by electron micros

96 ted by pathogenic antibodies, including anti-glomerular basement membrane disease and lupus nephritis

97 acrophage- and T-cell-mediated model of anti-glomerular basement membrane disease in STC1 transgenic

98 phritis (APTN) is an aggressive form of anti-glomerular basement membrane disease that targets the al

99 P), 8; systemic lupus erythematosus, 3; Anti-glomerular basement membrane disease, 2; oxalosis, 2; an

100 asmic antibodies-associated vasculitis, anti-glomerular basement membrane disease, and systemic lupus

101 e glomerulonephritis after induction of anti-glomerular basement membrane disease, with more infiltra

102 roach to the treatment of patients with anti-glomerular basement membrane disease.

103 In Goodpasture's (anti-glomerular basement membrane) disease, autoimmunity to t

104 findings included segmental splitting of the glomerular basement membrane, effacement of podocyte foo

105 owed abundant IgG deposition in the expanded glomerular basement membrane, especially in regions corr

106 er fixation of nephrotoxic antibodies to the glomerular basement membrane, even in the absence of pro

107 l role of tight adhesion of podocytes to the glomerular basement membrane for maintaining glomerular

108 ned at autopsy, glomeruli were isolated, and glomerular basement membrane fragments were prepared.

109 disease was the appearance of bare areas of glomerular basement membrane from the pulling apart of p

110 The anti-glomerular basement membrane (GBM) Ab has been regarded

111 ns that are seen at onset of albuminuria are glomerular basement membrane (GBM) alterations with a si

112 f laminin alpha5 results in breakdown of the glomerular basement membrane (GBM) and failed glomerular

113 s considerable evidence implicating both the glomerular basement membrane (GBM) and the epithelial fi

114 pecialized extracellular matrix known as the glomerular basement membrane (GBM) and the podocyte foot

115 noperoxidase assay on cell layers using anti-glomerular basement membrane (GBM) antibodies.

116 moattractant, during the progression of anti-glomerular basement membrane (GBM) antibody (Ab) GN, a m

117 Anti-glomerular basement membrane (GBM) antibody nephritis is

118 lammation and in the progression of the anti-glomerular basement membrane (GBM) antibody-induced expe

119 een immunized with a recombinant form of the glomerular basement membrane (GBM) antigen, Col4alpha3NC

120 ns of alpha3alpha4alpha5(IV) collagen in the glomerular basement membrane (GBM) are targets of Goodpa

121 Ultrastructural changes in the glomerular basement membrane (GBM) at 2 weeks of age res

122 aminin alpha5 replaces laminin alpha1 in the glomerular basement membrane (GBM) at the capillary loop

123 f the alpha3/4/5(IV) collagen network in the glomerular basement membrane (GBM) cause Alport syndrome

124 ixon, my work examined how antibodies to the glomerular basement membrane (GBM) cause disease.

125 Primary defects in either podocytes or the glomerular basement membrane (GBM) cause proteinuria, a

126 r 500-fold increase in albuminuria), loss of glomerular basement membrane (GBM) charge and foot proce

127 Here we have determined in human skin and glomerular basement membrane (GBM) collagen the levels o

128 Expression of glomerular basement membrane (GBM) collagens is reduced

129 e were less adherent than wild-type cells to glomerular basement membrane (GBM) components collagen I

130 Alport syndrome is a glomerular basement membrane (GBM) disease caused by mut

131 Anti-glomerular basement membrane (GBM) disease is a rapidly

132 Human anti-glomerular basement membrane (GBM) disease strongly asso

133 We developed a new mouse model of human anti-glomerular basement membrane (GBM) disease to better cha

134 We developed a rat model of human anti-glomerular basement membrane (GBM) disease to investigat

135 n G (IgG) and complement C3, typical of anti-glomerular basement membrane (GBM) disease.

136 macrophage-mediated, cytokine-dependent anti-glomerular basement membrane (GBM) glomerulonephritis (G

137 logous phase of an accelerated model of anti-glomerular basement membrane (GBM) glomerulonephritis us

138 mmation, the development of accelerated anti-glomerular basement membrane (GBM) glomerulonephritis wa

139 star Kyoto rats by a single injection of rat glomerular basement membrane (GBM) in adjuvant.

140 gle injection of collagenase-solubilized rat glomerular basement membrane (GBM) in adjuvant.

141 yoto (WKY) rats by a single injection of rat glomerular basement membrane (GBM) in adjuvant.

142 the kidney adhere tightly to the underlying glomerular basement membrane (GBM) in order to maintain

143 The glomerular basement membrane (GBM) is a specialized extr

144 of alpha3, alpha4, and alpha5 chains in the glomerular basement membrane (GBM) is speculated to invo

145 Linear binding of IgG to the glomerular basement membrane (GBM) is the hallmark of an

146 e replaced by immigration of cells along the glomerular basement membrane (GBM) is under debate.

147 ivo, we induced a model of Fc-dependent anti-glomerular basement membrane (GBM) nephritis in wild-typ

148 Alport posttransplantation anti-glomerular basement membrane (GBM) nephritis is mediated

149 monitor renal disease progression in an anti-glomerular basement membrane (GBM) nephritis mouse model

150 significant structural abnormalities in the glomerular basement membrane (GBM) of diabetic individua

151 The ultrafiltration function of the glomerular basement membrane (GBM) of the kidney is impa

152 tion with either collagenase-solubilized rat glomerular basement membrane (GBM) or the recombinant NC

153 rats immunized with collagenase-solubilized glomerular basement membrane (GBM) or the recombinant NC

154 Glomerular basement membrane (GBM) plays a crucial funct

155 Abnormal permselectivity of glomerular basement membrane (GBM) plays an important ro

156 Detachment of podocytes from the glomerular basement membrane (GBM) rather than apoptosis

157 nbred strains of mice with rabbit anti-mouse glomerular basement membrane (GBM) reactive sera.

158 psy, immunofluorescence (IF) showed granular glomerular basement membrane (GBM) staining for C4d, IgG

159 It is the kidney glomerular basement membrane (GBM) that is defective in

160 We used an ELISA employing extracts of human glomerular basement membrane (GBM) to detect, characteri

161 ed in diabetic patients, but surface area of glomerular basement membrane (GBM) underlying the podocy

162 Glomerular basement membrane (GBM) width (356 +/- 52 ver

163 All three groups had increased glomerular basement membrane (GBM) width and mesangial f

164 Mesangial and matrix volume fractions and glomerular basement membrane (GBM) width were increased

165 nked heparan sulfate (HS) alterations in the glomerular basement membrane (GBM) with albuminuria as a

166 r organization of proteins within the kidney glomerular basement membrane (GBM), an essential mediato

167 lial cell loss, double-contour appearance of glomerular basement membrane (GBM), and thrombus formati

168 teins and neutral dextrans permeate into the glomerular basement membrane (GBM), in general agreement

169 mers of alpha3(IV) collagen that bind to the glomerular basement membrane (GBM), usually causing rapi

170 mponent of the renal filtration barrier--the glomerular basement membrane (GBM)--can disassemble cati

171 h proteinuria, decreased renal function, and glomerular basement membrane (GBM)-bound deposits in hal

172 jected to an augmented passive model of anti-glomerular basement membrane (GBM)-induced experimental

173 rastructural thickening and splitting of the glomerular basement membrane (GBM).

174 us-1 (NC1) domain of type IV collagen in the glomerular basement membrane (GBM).

175 nely clog with large proteins that enter the glomerular basement membrane (GBM).

176 which form the collagenous network of mature glomerular basement membrane (GBM).

177 heparan sulfate proteoglycans (HSPGs) in the glomerular basement membrane (GBM).

178 rs of plasma every day through a specialized glomerular basement membrane (GBM).

179 of C3 within the kidney, commonly along the glomerular basement membrane (GBM).

180 target the alpha3(IV) collagen chain in the glomerular basement membrane (GBM).

181 glomerulogenesis associated with an abnormal glomerular basement membrane (GBM).

182 inin beta2 (LAMB2), a major component of the glomerular basement membrane (GBM).

183 h forms the major collagen IV network of the glomerular basement membrane (GBM).

184 they remove Ig and immune complexes from the glomerular basement membrane (GBM).

185 ma1) trimer, an important constituent of the glomerular basement membrane (GBM).

186 with specific ultrastructural lesions of the glomerular basement membrane (GBM).

187 a4alpha5(IV) networks found in mature kidney glomerular basement membrane (GBM).

188 21, which is an important constituent of the glomerular basement membrane (GBM).

189 3(IV) collagen, an integral component of the glomerular basement membrane (GBM); this effect was comp

190 preparations of skin collagen (n = 110) and glomerular basement membrane (GBM, n = 28) were enzymati

191 or AGE detected in diabetic mesangium (96%), glomerular basement membranes (GBM) (42%), tubular basem

192 TEM analysis of the glomerular basement membranes (GBM) during development o

193 Laminin alpha2 chain was absent from glomerular basement membranes (GBM) in normal human, mur

194 Why glomerular basement membranes (GBM) undergo laminin tran

195 spread podocyte foot process broadening, and glomerular basement membranes (GBMs) were significantly

196 glomerulonephritis after induction with anti-glomerular basement membrane globulin, with enhanced pat

197 cal characteristics during experimental anti-glomerular basement membrane glomerulonephritis (anti-GB

198 e compared the intensity of accelerated anti-glomerular basement membrane glomerulonephritis between

199 diffuse type that is characteristic of anti-glomerular basement membrane glomerulonephritis, and a f

200 Anti-glomerular basement membrane GN involved NET formation a

201 Accelerated anti-glomerular basement membrane GN was examined in groups o

202 monomers, but not dimers, from native human glomerular basement membrane hexamers, a property that m

203 proteinuria and decreased renal function and glomerular basement membrane IgG deposits.

204 einuria and restored the architecture of the glomerular basement membrane in alpha1 integrin-null Alp

205 novel podocyte protrusions invading into the glomerular basement membrane in disease and these occurr

206 we found striking ultrastructural changes in glomerular basement membranes in FVB mice.

207 Ultrastructural abnormalities of the glomerular basement membrane, including lamellation and

208 r neutrophil accumulation and damage in anti-glomerular basement membrane-induced (anti-GBM-induced)

209 Similarly, both anti-glomerular basement membrane-induced glomerulonephritis

210 ous chronic glomerulonephritis (GN) and anti-glomerular basement membrane-induced nephritis.

211 ment of viable podocytes from the underlying glomerular basement membrane is an important mechanism o

212 glomerular epithelial cell attachment to the glomerular basement membrane is an important pathogeneti

213 , the improvement in the architecture of the glomerular basement membrane is associated with de novo

214 Because podocyte adhesion to the glomerular basement membrane is mediated by integrins, t

215 Podocyte adhesion to the glomerular basement membrane is required for proper func

216 Ultrastructural studies show that the glomerular basement membrane is thickened, podocyte slit

217 llagen IV networks, a major component of the glomerular basement membrane, is poorly understood.

218 onstrate that defects induced by proteins of glomerular basement membrane lead to an insidious plasma

219 ed by lipopolysaccharide and antibody to the glomerular basement membrane, led to rapid glomerular ne

220 led histopathological analysis revealed that glomerular basement membrane lesions typical of Alport s

221 te that was adsorbed to NC1 hexamer from rat glomerular basement membrane lost all reactivity to glom

222 tration slit frequency and thickening of the glomerular basement membrane, lowering computed hydrauli

223 on gel behavior show that proteins cross the glomerular basement membrane mainly by diffusion rather

224 We used lupus and anti-glomerular basement membrane models of nephritis to dete

225 nally inhibited, glomerular foot process and glomerular basement membrane morphology are primarily re

226 lomerulonephritis, type I and II (MPG), anti-glomerular basement membrane nephritis (anti-GBM), and m

227 dedifferentiated podocytes of mice with anti-glomerular basement membrane nephritis and in human immu

228 Using anti-glomerular basement membrane nephritis in rats, we inves

229 Moreover, after induction of anti-glomerular basement membrane nephritis in young mice, iP

230 ssary for local chemokine expression in anti-glomerular basement membrane nephritis, although the dif

231 ntrol mice, were challenged with rabbit anti-glomerular basement membrane nephrotoxic sera (NTS), to

232 inin-2 and/or laminin-4) accumulating in the glomerular basement membrane of Alport mice is markedly

233 tive assembly of the alpha3(IV) chain in the glomerular basement membrane of patients with Alport syn

234 abnormal electron-dense material within the glomerular basement membrane of the kidney and often wit

235 emonstrate that severe defects in either the glomerular basement membrane or the glomerular endotheli

236 f type IV collagen, the major constituent of glomerular basement membrane, or LMX1B transcription fac

237 effacement, irregular and split areas of the glomerular basement membrane, podocyte apoptosis and dep

238 of glomerular epithelial slit diaphragm and glomerular basement membrane proteins implicated in glom

239 circulating proteins and AGE modification of glomerular basement membrane proteins may both contribut

240 y inflammation in a macrophage-mediated anti-glomerular basement membrane reactive serum-induced immu

241 Sub-threshold doses of glomerular basement membrane-reactive serum induced more

242 The interface between the podocyte and the glomerular basement membrane requires integrins, and def

243 e glomerular epithelial cell detachment from glomerular basement membrane seen in the PAN nephrosis m

244 netic model of podocyte injury and segmental glomerular basement membrane splitting due to hyposialyl

245 pathy with podocyte effacement and segmental glomerular basement membrane splitting due to hyposialyl

246 ysms, glomerular hypertrophy, podocyte loss, glomerular basement membrane splitting, and secondary fo

247 ollagen IV networks, which are essential for glomerular basement membrane stability and molecular ult

248 sting that modifier genes act by influencing glomerular basement membrane structure.

249 n the kidneys each consisting of a barrel of glomerular basement membrane surrounded by glomerular en

250 more prominent immune deposits and a thicker glomerular basement membrane than at baseline.

251 is, and changes in the ultrastructure of the glomerular basement membrane that increase in severity i

252 l development of dorsal limb structures, the glomerular basement membrane, the anterior segment of th

253 follows: 9/14 had moderate or severe diffuse glomerular basement membrane thickening and 2/14 had nod

254 A expression down-regulation and ameliorated glomerular basement membrane thickening and foot process

255 Transmission electron microscopy revealed glomerular basement membrane thickening and podocyte eff

256 histology revealed mesangial expansion, and glomerular basement membrane thickening as determined by

257 Glomerular basement membrane thickening depended on incr

258 Diabetic glomerular basement membrane thickening was prevented in

259 hypertrophy, mesangial matrix accumulation, glomerular basement membrane thickening, albuminuria, an

260 ar thickening, tubular dilation and atrophy, glomerular basement membrane thickening, and mesangial e

261 icroalbuminuria, mesangial matrix expansion, glomerular basement membrane thickening, and podocyte lo

262 es that exhibits mesangial matrix expansion, glomerular basement membrane thickening, and renal insuf

263 d many DN features, including podocyte loss, glomerular basement membrane thickening, mesangial expan

264 inary albumin excretion, glomerulosclerosis, glomerular basement membrane thickening, mitochondrial D

265 megaly, mesangial sclerosis, cast formation, glomerular basement membrane thickening, podocyte efface

266 Diabetes-induced mesangial expansion, glomerular basement membrane thickening, podocyte foot-p

267 oteinuria, fewer IgG glomerular deposits, no glomerular basement membrane thickening, reduced levels

268 illary surface area remained stable, but the glomerular basement membrane thickness was increased and

269 lbuminuria, arteriolar hyalinosis, increased glomerular basement membrane thickness, mesangial expans

270 Compared with wild-type mice, after anti-glomerular basement membrane treatment STC1 transgenic m

271 chemical and mechanical signals to/from the glomerular basement membrane upon which it elaborates, a

272 They stay attached to the glomerular basement membrane via integrin interactions t

273 The glomerular basement membrane was disorganized and glomer

274 their suitability as experimental models of glomerular basement membrane was examined by measuring t

275 Glomerular basement membrane was thickened in OVE26 mice

276 ynthetic gels were quite similar to those in glomerular basement membrane, when compared on the basis

277 tion of extracellular chromatin fragments in glomerular basement membranes where they appear in compl

278 ey diabetic subject groups, respectively, in glomerular basement membrane width (median [range] 511 n

279 uminuria, mesangial expansion, and increased glomerular basement membrane width in diabetic mice.

280 these patients with type 1 diabetes who had glomerular basement membrane widths within the normal ra