ライフサイエンスコーパス: mesangial

1 atterns were diffuse (53%), focal (28%), and mesangial (13%) proliferative glomerulonephritis.

2 Mesangial and circulating IgA1 with aberrantly glycosyla

3 barrier of the glomerulus/glomus and recruit mesangial and endothelial cells to form a mature glomeru

4 complete globotriaocylceramide clearance of mesangial and glomerular endothelial cells across all do

5 Pathologic proliferation of mesangial and parietal epithelial cells (PECs) is a hall

6 or blood pressure, EOCs not only attenuated mesangial and peritubular matrix expansion, as well as t

7 Only in 26-week allografts, we found mesangial and subendothelial immune complex-type electro

8 creased lysine acetylation was also noted in mesangial and tubular cells exposed to 25 mmol/L compare

9 ions, reduced migration and proliferation in mesangial and tubuloepithelial cells, and altered the ex

10 eceptor subtypes on endothelial, epithelial, mesangial, and inflammatory cells have been implicated i

11 s pathophysiologic crosstalk that influences mesangial architecture and sclerosis.

12 rast, subtotal FH deficiency associated with mesangial C3 accumulation consistent with C3G.

13 ment membrane and triggers the appearance of mesangial C3 deposits in CFH(-/-) mice; here, we show th

14 Glomerular mesangial cell (GMC) proliferation and death are involve

15 Glomerular mesangial cell (GMC) proliferation and matrix expansion

16 mune complexes are capable of inducing human mesangial cell (HMC) activation, resulting in release of

17 loop facilitating IgA1-sCD89 deposition and mesangial cell activation, thus identifying TGase2 as a

18 logical conditions associated with decreased mesangial cell alphavbeta8 expression and TGF-beta secre

19 gial-to-endothelial cell cross-talk, whereby mesangial cell alphavbeta8 homeostatically arbitrates gl

20 s collagen I deposition in vivo and promotes mesangial cell apoptosis in vitro.

21 Mesangial cell attachment to collagen I led to increased

22 Hic-5 expression increases following mesangial cell attachment to collagen I, associated with

23 Imaging of mesangial cell cultures and analysis of detergent-insolu

24 Adding exogenous TGF-beta to mesangial cell cultures failed to increase Hic-5 express

25 Mesangial cell cultures treated with poly(I:C) or tunica

26 icroalbuminuria, glomerular filtration rate, mesangial cell expansion, and collagen type IV and trans

27 In addition, mesangial cell exposure to alpha4-containing laminins, b

28 Mesangial cell expression of the LIM protein hydrogen pe

29 ling in stromal progenitors is essential for mesangial cell formation but is dispensable for the smoo

30 We propose that diabetic ECM affects mesangial cell functions via two distinct mechanisms: mo

31 ajor features of the diabetic milieu, affect mesangial cell functions.

32 Mesangial cell Hic-5 expression was associated with incr

33 0, resulting in the inhibition of mTORC1 and mesangial cell hypertrophy and fibronectin and PAI-1 exp

34 These mechanisms may contribute to mesangial cell hypertrophy and matrix expansion in DN.

35 cose-induced Akt acts as a signaling hub for mesangial cell hypertrophy and matrix expansion, which a

36 ase expression, leading to increased ROS and mesangial cell hypertrophy and matrix protein expression

37 olving these signaling molecules to regulate mesangial cell hypertrophy are not fully understood.

38 mediated inhibition of protein synthesis and mesangial cell hypertrophy induced by TGFbeta.

39 TOR) promote increased protein synthesis and mesangial cell hypertrophy.

40 regulation and TORC1/2 activation in driving mesangial cell hypertrophy.

41 otal clearance of glomerular endothelial and mesangial cell inclusions, and findings from 2 patients

42 Mesangial cell injury has a major role in many CKDs.

43 lts in mesangial cell proliferation, whereas mesangial cell injury leads to foot process fusion and p

44 Overexpression of Far2 in a mouse mesangial cell line induced upregulation of platelet act

45 ndant LacZ-expressing cells colocalized with mesangial cell markers alpha8-integrin and PDGF receptor

46 family member CCN2 to inhibit fibrosis in a mesangial cell model of DN.

47 nvestigated whether Hic-5-induced changes in mesangial cell phenotype were TGF-beta-dependent.

48 bitor or deletion of integrin alpha1 reduced mesangial cell process invasion of the glomerular capill

49 integrin alpha1beta1-dependent Rac1-mediated mesangial cell process invasion of the glomerular capill

50 L-NAME salt-induced hypertension accelerated mesangial cell process invasion.

51 IgA nephropathy (IgAN) is characterized by mesangial cell proliferation and extracellular matrix ex

52 of glomeruli from animals with VL identified mesangial cell proliferation and interposition.

53 ritis model, roscovitine treatment decreased mesangial cell proliferation and matrix proteins [1].

54 nd platelet-derived growth factor-stimulated mesangial cell proliferation and promotes IL-6 productio

55 Endothelin-1 promotes mesangial cell proliferation and sclerosis.

56 Additionally, costimulation enhanced mesangial cell proliferation compared with each stimulan

57 se and increased in glomeruli and serum when mesangial cell proliferation subsides.

58 At day 7, CCN3 overexpression decreased mesangial cell proliferation, including expression of al

59 In contrast to factors that promote mesangial cell proliferation, little is known about thei

60 r B (PDGF-B) signaling has a pivotal role in mesangial cell proliferation, we examined the regulatory

61 s that podocyte injury frequently results in mesangial cell proliferation, whereas mesangial cell inj

62 to inhibition or promotion, respectively, of mesangial cell proliferation.

63 et of PDGF-B signaling and a key mediator of mesangial cell proliferation.

64 tribution of TxNIP was investigated in renal mesangial cell reactive oxygen species (ROS) generation

65 Thus, mesangial cell research still holds much promise.

66 Therefore, modulation of mesangial cell responses would offer a pathophysiology-b

67 sis was induced by administration of an anti-mesangial cell serum in combination with LPS.

68 l, redundant function for Notch receptors in mesangial cell specification, proliferation or survival

69 ivation with C3b and C5b-9 deposition on the mesangial cell surface in vitro This gain of function in

70 injury by inhibiting apoptosis and promoting mesangial cell survival.

71 provides endothelial cytoprotection against mesangial cell TGF-beta.

72 In vivo, vascular smooth muscle cell/mesangial cell-specific overexpression of Nox5 in a mous

73 In human mesangial cells (a microvascular pericyte that secretes

74 ein), parietal epithelial cells (PAX 8), and mesangial cells (alpha8 integrin).

75 arly" during adult life from 2 to 24 months: mesangial cells (e.g., MMP9), endothelial cells (e.g., I

76 gated in an in vitro model using human renal mesangial cells (HRMCs).

77 Moreover, immortalized human mesangial cells (ihMCs) exposed to high glucose (HG) lev

78 ming growth factor-beta1 (TGF-beta) in renal mesangial cells (MC) are hallmark features of diabetic n

79 To determine the role of TxNIP, mouse mesangial cells (MC) cultured from wild-type C3H and TxN

80 Activation of glomerular mesangial cells (MCs) by angiotensin II (Ang II) leads t

81 Integrin alpha1-null mesangial cells (MCs) have reduced Cav-1 levels, and ree

82 Aberrant proliferation of mesangial cells (MCs) is a key finding in progressive gl

83 Here, we demonstrate that, in glomerular mesangial cells (MCs), endothelial nitric oxide synthase

84 ) and the contractile function of glomerular mesangial cells (MCs).

85 apidly induced autophagy within 1 h in mouse mesangial cells (MMC) as determined by increased microtu

86 knockdown by specific siRNA in primary mouse mesangial cells (MMC), resulted in increased protein lev

87 betic mice as well as TGF-beta-treated mouse mesangial cells (MMC).

88 e (HG)- or TGF-beta-treated mouse glomerular mesangial cells (MMCs).

89 Growth-arrested rat mesangial cells (RMCs) at a G0/G1 interphase stimulated

90 Renal mesangial cells (RMCs) constitute a population of cells

91 miR302 overexpressing mesangial cells also exhibited enhanced expression of EZ

92 ease in integrin alpha1 expression in Alport mesangial cells and an increase in integrin alpha3 in Al

93 r, these data demonstrate a unique origin of mesangial cells and demonstrate a novel, redundant funct

94 glomerulus, a capillary network supported by mesangial cells and extracellular matrix (ECM).

95 Nox5 in human diabetic nephropathy in human mesangial cells and in an inducible human Nox5 transgeni

96 icroRNA-192 (miR-192) in cultured glomerular mesangial cells and in glomeruli from diabetic mice.

97 ritical role for GATA3 in the maintenance of mesangial cells and its absolute requirement for prevent

98 (i) Immunoblot analysis in cultured mesangial cells and kidney cortex revealed that Nox4 is

99 ATA3 is specifically expressed in glomerular mesangial cells and plays a critical role in the mainten

100 Mesangial cells and podocytes express integrins alpha1be

101 e alpha8 integrin chain is expressed only on mesangial cells and vascular smooth muscle cells.

102 w that glomerular podocytes, renal GECs, and mesangial cells are permissive for ZIKV infection.

103 Renal mesangial cells are responsible for glomerular PAF gener

104 Mesangial cells are specialized pericyte/smooth muscle c

105 ymerase II recruitment to these promoters in mesangial cells as well as in glomeruli that were purifi

106 ix show that, under high glucose conditions, mesangial cells assembled significantly more FN matrix,

107 in this process, as individual mutants have mesangial cells at birth.

108 However, inducing Hic-5 expression in mesangial cells by adhesion to collagen I led to TGF-bet

109 ow that TGF-beta activates Akt in glomerular mesangial cells by inducing miR-200b and miR-200c, both

110 merular endothelial cells and TGF-beta1 from mesangial cells cocultured with glomerular endothelial c

111 In vitro studies of human and rat mesangial cells confirmed a stimulatory effect of PDGF-B

112 ificantly reduced in diabetic kidneys and in mesangial cells cultured from Fcgamma receptor-deficient

113 r transcripts are increased in podocytes and mesangial cells cultured in elevated glucose compared wi

114 Mesangial cells cultured under high glucose conditions p

115 Itgb8(-/-) mesangial cells demonstrated reduced latent TGF-beta bin

116 hat there is a prosclerotic feedback loop in mesangial cells dependent on matrix-derived signals in w

117 renin-positive precursor cells give rise to mesangial cells during nephrogenesis, this study tested

118 t pronephric development the interglomerular mesangial cells exhibit numerous cytoplasmic granules, w

119 We show that cultured rat mesangial cells express CCN3 mRNA and protein, and that

120 Mesangial cells expressing Hic-5 showed altered latent T

121 a1 induces autophagy and protects glomerular mesangial cells from undergoing apoptosis during serum d

122 Whether mesangial cells have a distinct origin from vascular smo

123 th muscle cells and pericytes and glomerular mesangial cells in the kidney and that Tbx18-expressing

124 in wild-type, but not integrin alpha2-null, mesangial cells in vitro, demonstrating that its effects

125 eas adding TGF-beta to siRNA Hic-5 knockdown mesangial cells increased procollagen I transcription to

126 Knockdown of Sgpl1 in rat mesangial cells inhibited cell migration, which was part

127 that govern PAF metabolism and signaling in mesangial cells is important, because it could facilitat

128 pithelial cells, but the function of DbpA in mesangial cells is unknown.

129 ion between IgA1, sCD89, TfR1, and TGase2 on mesangial cells needed for disease development.

130 The M4 protein was demonstrated to bind to mesangial cells not via the IgA-binding region but rathe

131 We previously reported that TxNIP-deficient mesangial cells showed protection from HG-induced reacti

132 Cultured mesangial cells showed reduced migratory potential when

133 vitro experiments with perlecan-positive rat mesangial cells showed that FGF2-induced proliferation i

134 Expression of IRS1 mutant Arg972 in human mesangial cells significantly reduced the insulin-stimul

135 s showed: (i) that growth-arrested G0/G1 rat mesangial cells stimulated to divide in hyperglycemic me

136 WT bone marrow-derived macrophages and renal mesangial cells stimulated with S100A8/A9 secrete IL-6,

137 How mesangial cells sustain the activated state of Akt is no

138 mediator in regulating responses of dividing mesangial cells to hyperglycemia.

139 e gene expression profile of ET-1-stimulated mesangial cells to identify determinants of collagen acc

140 amma in the absence of its ligand sensitized mesangial cells to TNF-alpha stimulation.

141 PRA) gene transcription, using primary mouse mesangial cells treated with class-specific HDAC inhibit

142 in the glomeruli of mouse models of DN, and mesangial cells treated with transforming growth factor-

143 in TGF-beta1-mediated ECM gene expression in mesangial cells under normal and HG conditions.

144 in TGF-beta1-induced gene expression in rat mesangial cells under normal and high-glucose (HG) condi

145 timulation induced proliferation of PECs and mesangial cells via CD74.

146 In vitro, silencing of Nox5 in human mesangial cells was associated with attenuation of the h

147 nt increases in the number of Ki-67-positive mesangial cells were also found, but glomerular WT1 expr

148 Cultured rat mesangial cells were exposed to high glucose (25 mmol/L)

149 differentiation of smooth muscle, renin, and mesangial cells were impaired.

150 Primary rat mesangial cells were treated with high glucose (30 mm) o

151 Previously, we found that treatment of mesangial cells with anti-DNA antibodies induced high ex

152 Costimulation of human mesangial cells with M4 and galactose-deficient polymeri

153 Prolonged incubation of mesangial cells with TGFbeta reduced the levels of depto

154 nal glomerular endothelial cells (GECs), and mesangial cells with ZIKV.

155 support cells termed podocytes, perivascular mesangial cells, and parietal epithelial cells.

156 , we exposed proximal tubular cells, primary mesangial cells, and podocytes to TGF-beta1 to examine i

157 IgA1 enhanced binding of M4 to mesangial cells, but not vice versa.

158 ealed that podocytes, but not endothelial or mesangial cells, contain collagen alpha 3 alpha 4 alpha

159 in vitro but was not taken up efficiently by mesangial cells, glomerular endothelial cells, or proxim

160 In cultured human mesangial cells, H2O2 and TNF-alpha inhibited TRPC6 mRNA

161 In renal mesangial cells, high glucose increased the expression o

162 In human renal mesangial cells, high glucose induced ROS production and

163 roximately 5000 gene promoters in glomerular mesangial cells, including those of Tgfb1, Tgfb3, and Ct

164 e complexes induce proliferation of resident mesangial cells, increased production of extracellular m

165 uding cortical type 1 fibroblast-like cells, mesangial cells, macrophages, and dendritic cells, showe

166 In mouse mesangial cells, PFD decreased TGF-beta promoter activit

167 ed with structural and functional changes of mesangial cells, podocytes, and proximal tubular cells t

168 ycemia, which led to TrkA phosphorylation in mesangial cells, tubular epithelial cells, and podocytes

169 the activation and proliferation of PECs and mesangial cells, whereas wild-type mice were not.

170 Kidney alphavbeta8 localizes to mesangial cells, which appose glomerular endothelial cel

171 ce showed degenerative changes in glomerular mesangial cells, which deteriorated progressively during

172 uces ADAM17 transcriptional up-regulation in mesangial cells, which is associated with augmentation o

173 protein-1 expression induced by TNF-alpha in mesangial cells, which was dependent on NF-kappaB signal

174 localization demonstrated Nox5 expression in mesangial cells.

175 glucose-induced matrix production by kidney mesangial cells.

176 mmatory responses and proliferation of human mesangial cells.

177 brotic proteins in both proximal tubular and mesangial cells.

178 RK1/2, p38), and collagen IV accumulation in mesangial cells.

179 aled SGPL1 expression in mouse podocytes and mesangial cells.

180 d the induction of MCP-1 by palmitic acid in mesangial cells.

181 model in Nrf2(-/-) mice, and cultured human mesangial cells.

182 matory cytokine expression in rat glomerular mesangial cells.

183 calized inflammatory responses by activating mesangial cells.

184 d TGF-beta1-induced TAK1 activation in mouse mesangial cells.

185 ing activation and proliferation of PECs and mesangial cells.

186 ovo in PECs and colocalized in both PECs and mesangial cells.

187 he development and maintenance of glomerular mesangial cells.

188 ailed to direct sufficient GATA3 activity to mesangial cells.

189 seen in both mouse embryonic fibroblasts and mesangial cells.

190 H3 and H4- acetylation in primary glomerular mesangial cells.

191 ation was explored in vitro using glomerular mesangial cells.

192 duced profibrogenic responses in primary rat mesangial cells.

193 es at 72 hours, compared with renal GECs and mesangial cells.

194 ed macrophages, renal endothelial cells, and mesangial cells.

195 ve RT-PCR did not detect APOL1 mRNA in human mesangial cells; however, abundant levels of APOL1 mRNA

196 on in the engrafted kidney was predominantly mesangial, compared with a predominance of proliferative

197 bpA protein expression within the glomerular mesangial compartment in mesangioproliferative nephritis

198 ced DbpA expression predominantly within the mesangial compartment.

199 ter the vascular cleft and cannot rescue the mesangial deficiency.

200 IgA1 mesangial deposition is the hallmark of IgA nephropathy

201 accompanied with thrombus formation, whereas mesangial deposition of vWF was associated with mesangia

202 IgA1 that had different variable regions and mesangial deposition patterns indicated that, independen

203 hich produces polyclonal human IgA1 prone to mesangial deposition.

204 lusion, IgA1P strongly diminishes human IgA1 mesangial deposits and reduces inflammation, fibrosis, a

205 tor bearing the same IgA allotype, developed mesangial deposits consisting of IgA, IgG2a, and C3.

206 uman IgA1 and CD89 displayed circulating and mesangial deposits of IgA1-sCD89 complexes resulting in

207 One individual with mild mesangial disease had no significant change in activity

208 Pathological changes in diabetes include mesangial expansion and accumulation of extracellular ma

209 showed a borderline association between mild mesangial expansion and decreased risk for ESRD (subdist

210 lomerular fibrosis, as determined by altered mesangial expansion and deposition of laminin.

211 ess, proteinuria, glomerular hypertrophy and mesangial expansion in diabetic mice.

212 nce between septic and nonseptic animals was mesangial expansion on electron microscopy.

213 macrophage accumulation but had no effect on mesangial expansion or podocyte numbers.

214 e actions and exhibited more albuminuria and mesangial expansion than diabetic controls.

215 rstitial collagen deposition, but glomerular mesangial expansion was unaffected.

216 p<0.01), while urinary albumin excretion and mesangial expansion were reduced in diabetic CTGF+/- ani

217 albumin-to-creatinine ratio) and structural (mesangial expansion) glomerular injury and improves rena

218 These effects were associated with reduced mesangial expansion, accumulation of the extracellular m

219 protected from diabetes-induced hypertrophy, mesangial expansion, and albuminuria and failed to activ

220 production, accelerated glomerulosclerosis, mesangial expansion, and ECM protein (collagen IV and fi

221 al disease, such as foot process effacement, mesangial expansion, and glomerulosclerosis.

222 as expression of GqQ>L promoted albuminuria, mesangial expansion, and increased glomerular basement m

223 ss, glomerular basement membrane thickening, mesangial expansion, and proteinuria in nondiabetic youn

224 ignificant foot-process effacement, moderate mesangial expansion, and segmental thickening of the glo

225 d proteinuria and prevented podocyte injury, mesangial expansion, and tubulointerstitial fibrosis.

226 d with histologic features seen in LN, i.e., mesangial expansion, capillary proliferation, crescent f

227 type, many features of diabetic nephropathy (mesangial expansion, elevated plasma creatinine and urea

228 -777 decreased proteinuria, podocyte injury, mesangial expansion, fibrosis, and CD68 macrophage infil

229 RAGE deletion attenuated mesangial expansion, glomerular matrix accumulation, and

230 ice, characterized by increased albuminuria, mesangial expansion, glomerular matrix deposition, and t

231 Urinary albumin excretion, mesangial expansion, glomerulosclerosis, mesangiolysis,

232 a-deficient mice had enlarged glomeruli with mesangial expansion, injury, and FSGS at study end.

233 ob/ob mice was safe and reduced albuminuria, mesangial expansion, kidney weight, and cortical cholest

234 ent decreases in albuminuria, renal lesions (mesangial expansion, leukocyte infiltration, and fibrosi

235 sed albuminuria with glomerular enlargement, mesangial expansion, mesangiosclerosis, and expansion of

236 reased urinary albumin excretion with marked mesangial expansion, podocyte injury and apoptosis, but

237 , albuminuria, and renal histologic changes (mesangial expansion, tubular injury, and fibrosis) over

238 angial volume expansion and up-regulation of mesangial fibronectin expression, which is mediated by a

239 In separate analyses, mesangial fractional volume was lower in subjects treate

240 Differences in mesangial fractional volume were not estimated in the co

241 cardium, or kidney; but did produce cortical mesangial glomerulosclerosis.

242 nd were the only group to exhibit glomerular mesangial hypercellularity.

243 by miR-200b/c, which can lead to glomerular mesangial hypertrophy in the progression of diabetic nep

244 -beta) plays an important role in glomerular mesangial hypertrophy.

245 Levels of mesangial IgA1 deposits and the binding partners of thes

246 IgA nephropathy (IgAN), characterized by mesangial IgA1 deposits, is a leading cause of renal fai

247 nto IgA1-expressing mouse recipients induced mesangial IgA1 deposits.

248 (sCD89) complexes and overexpression of the mesangial IgA1 receptor, TfR1 (transferrin receptor 1).

249 eptococcal M proteins colocalize with IgA in mesangial immune deposits in patients with IgAN.

250 o, and pathway components are present in the mesangial immunodeposits, including properdin and factor

251 ed endocapillary IgA1 deposition but neither mesangial injury nor kidney dysfunction.

252 Flk-sel overexpression caused mesangial injury with increased proliferation associated

253 rular regeneration after murine experimental mesangial injury.

254 e during the regenerative phase after severe mesangial injury.

255 area in the glomerular tufts increased after mesangial injury.

256 We conclude that overexpression of mesangial integrin alpha1 and podocyte vimentin and inte

257 potential, indicating a functional role for mesangial laminins in progression of Alport glomerular p

258 significantly reduced albuminuria and kidney mesangial matrix accumulation in the db/db mice model in

259 ced albuminuria, glomerular hypertrophy, and mesangial matrix accumulation in the F1 Akita model of D

260 Mesangial matrix accumulation is an early feature of glo

261 with DKD, including glomerular hypertrophy, mesangial matrix accumulation, glomerular basement membr

262 associated with renal damage, in particular mesangial matrix expansion (MME).

263 deposits in the mesangial matrix, diminished mesangial matrix expansion and extended lifespan.

264 ks of age reduced 24-h albumin excretion and mesangial matrix expansion and improved glomerular ultra

265 etic mice decreased albuminuria and improved mesangial matrix expansion and podocyte morphology.

266 Untreated db/db mice developed mesangial matrix expansion and tubular epithelial cell a

267 Albuminuria, mesangial matrix expansion, and glomerular hypertrophy w

268 albuminuria, glomerular basement thickening, mesangial matrix expansion, and hypertension, compared w

269 reduced whole kidney glomerular hypertrophy, mesangial matrix expansion, extracellular matrix accumul

270 diabetic nephropathy with microalbuminuria, mesangial matrix expansion, glomerular basement membrane

271 tic Fcgamma receptor-deficient mice had less mesangial matrix expansion, inflammatory cell infiltrati

272 n near-complete reversal of both structural (mesangial matrix expansion, mesangiolysis, basement memb

273 ed albuminuria, foot-process effacement, and mesangial matrix expansion.

274 etion, glomerular and renal hypertrophy, and mesangial matrix expansion.

275 angial deposition of vWF was associated with mesangial matrix expansion.

276 tigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice.

277 is and tubular atrophy (IFTA), 4.8% abnormal mesangial matrix increase, 32.0% abnormal arteriolar hya

278 betic nephropathy characterized by increased mesangial matrix protein (e.g., collagen) accumulation.

279 Glomerular hypertrophy and accumulation of mesangial matrix, characteristic of early DN, were prese

280 einuria, lowered collagen IV deposits in the mesangial matrix, diminished mesangial matrix expansion

281 nt membrane thickness and a >50% increase in mesangial matrix.

282 Early mesangial nephritis initiates a cascade of inflammatory

283 Mesangial pathology is widely acknowledged to reflect gl

284 in alpha2-deficient Alport mice show reduced mesangial process invasion, and cultured laminin alpha2-

285 We show mesangial processes invading the capillary loops of both

286 In this sample, 46 (32%) patients had mesangial proliferation, whereas endocapillary prolifera

287 bited high autoantibody levels and developed mesangial proliferative glomerulonephritis, which resemb

288 ic syndrome of minimal change disease (MCD), mesangial proliferative GN (MesGN), or FSGS may be poor

289 dney biopsy at the time of recurrence showed mesangial proliferative GN in eight patients and membran

290 Diffuse mesangial sclerosis (focally approaching nodular glomeru

291 of a genetic diagnosis, and FSGS or diffuse mesangial sclerosis on initial biopsy as well as age, se

292 of RAGE in OVE26 mice reduced nephromegaly, mesangial sclerosis, cast formation, glomerular basement

293 , features characteristic of FSGS, including mesangial sclerosis, podocyte foot process effacement, t

294 n early disease, which progressed to diffuse mesangial sclerosis, with reduced podocytes, widespread

295 ESRD-free survival rate was 21% for diffuse mesangial sclerosis.

296 sCD89-TfR1 interaction induced mesangial surface expression of TGase2 (transglutaminase

297 sition involved a direct binding of sCD89 to mesangial TfR1 resulting in TfR1 up-regulation.

298 hese results clarify a singular mechanism of mesangial-to-endothelial cell cross-talk, whereby mesang

299 In addition, dendrin ablation ameliorates mesangial volume expansion and up-regulation of mesangia

300 Furthermore, the mesangial vWF deposition was detectable in young eNOSKO