ライフサイエンスコーパス: mesangial

1 Mesangial and circulating IgA1 with aberrantly glycosyla

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

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

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

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

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

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

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

9 s pathophysiologic crosstalk that influences mesangial architecture and sclerosis.

10 ma membrane was also found in the glomerular mesangial area of type 1 diabetic mice in two different

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

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

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

14 Glomerular mesangial cell (GMC) proliferation and matrix expansion

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

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

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

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

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

20 Mesangial cell attachment to collagen I led to increased

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

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

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

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

25 Mesangial cell expression of the LIM protein hydrogen pe

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

27 The glycosaminoglycan heparin inhibits mesangial cell growth, but the molecular mechanism is un

28 Mesangial cell Hic-5 expression was associated with incr

29 ed the effects of high glucose, resulting in mesangial cell hypertrophy and expression of fibronectin

30 on of PRAS40 is required for TGFbeta-induced mesangial cell hypertrophy and fibronectin and collagen

31 Also, the acetylation mimetic attenuated the mesangial cell hypertrophy and fibronectin and collagen

32 0, resulting in the inhibition of mTORC1 and mesangial cell hypertrophy and fibronectin and PAI-1 exp

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

34 -mediated Akt/PRAS40 phosphorylation to spur mesangial cell hypertrophy and matrix protein accumulati

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

36 kinase deacetylation in high glucose-induced 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 Overexpression of Far2 in a mouse mesangial cell line induced upregulation of platelet act

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

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

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

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

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

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

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

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

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

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

54 Endothelin-1 promotes mesangial cell proliferation and sclerosis.

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

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

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

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

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

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

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

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

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

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

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

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

67 om Akita mice, csGRP78 co-localized with the mesangial cell surface marker alpha8-integrin.

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

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

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

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

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

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

74 lls, and a subset of these cells mature into mesangial cells (MCs) that continue to express GATA3 in

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

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

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

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

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

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

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

82 Here, rat mesangial cells (RMCs) were growth-arrested in the G(0)/

83 miR302 overexpressing mesangial cells also exhibited enhanced expression of EZ

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

85 ein levels and cGMP accumulation in cultured mesangial cells and attenuated ANP-mediated relaxation o

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

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

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

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

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

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

92 Mesangial cells and podocytes express integrins alpha1be

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

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

95 Renal mesangial cells are responsible for glomerular PAF gener

96 Mesangial cells are specialized pericyte/smooth muscle c

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

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

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

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

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

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

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

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

105 Mesangial cells cultured under high glucose conditions p

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

107 Previously, we showed that rat kidney mesangial cells dividing during hyperglycemic stress abn

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

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

110 Mesangial cells expressing Hic-5 showed altered latent T

111 We developed NPs that probe mesangial cells for the presence of angiotensin-converti

112 Whether mesangial cells have a distinct origin from vascular smo

113 ar endothelial cells, maps for podocytes and mesangial cells have not been available.

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

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

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

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

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

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

120 uited into the glomeruli and the damaged rat mesangial cells leads to diabetic nephropathy, fibrosis,

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

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

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

124 Cultured mesangial cells showed reduced migratory potential when

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

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

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

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

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

130 articularly suited for the identification of mesangial cells that play a pivotal role in diabetic nep

131 n and knockdown experiments in primary human mesangial cells to examine the glucose-mediated regulati

132 ther, IFN-lambda activates keratinocytes and mesangial cells to produce chemokines that induce immune

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

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

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

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

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

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

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

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

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

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

143 In mesangial cells, ACL is synergistically induced by high

144 seq dataset, including glomerular podocytes, mesangial cells, and endothelial cells.

145 on-associated mechano-sensory ion channel in mesangial cells, and identification of proximal tubule c

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

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

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

149 y were not stained by markers for podocytes, mesangial cells, endothelial cells, or proximal or loop

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

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

152 In mesangial cells, high glucose decreased the acetylation

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

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

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

156 GRP78 in HG-induced profibrotic responses in mesangial cells, informing a potential approach to treat

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

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

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

160 Novel marker genes and gene signatures of mesangial cells, vascular smooth muscle cells of the aff

161 Using primary kidney mesangial cells, we show that HG treatment, but not the

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

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

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

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

166 he development and maintenance of glomerular mesangial cells.

167 ailed to direct sufficient GATA3 activity to mesangial cells.

168 seen in both mouse embryonic fibroblasts and mesangial cells.

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

170 ation was explored in vitro using glomerular mesangial cells.

171 duced profibrogenic responses in primary rat mesangial cells.

172 complex proteins reduced binding to cultured mesangial cells.

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

174 mTORC1 activation downstream of PDGFRbeta 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 i that were composed mainly of podocytes and mesangial cells.

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

181 flammatory SMAD7 and IkappaBalpha factors in mesangial cells.

182 localization demonstrated Nox5 expression in mesangial cells.

183 aled SGPL1 expression in mouse podocytes and mesangial cells.

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

185 ne kinase expressed abundantly in glomerular mesangial cells.

186 ing activation and proliferation of PECs and mesangial cells.

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

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

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

190 ced DbpA expression predominantly within the mesangial compartment.

191 resence of characteristic subendothelial and mesangial curved, comma-like, banded collagen type 3 fib

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

193 ltered affinity maturation can influence IgA mesangial deposition and activate complement, we used se

194 IgA1 mesangial deposition is the hallmark of IgA nephropathy

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

196 N) often follows infections and features IgA mesangial deposition.

197 hich produces polyclonal human IgA1 prone to mesangial deposition.

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

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

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

201 uced by innate-like B cells might also yield mesangial deposits.

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

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

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

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

206 DUSP4 exacerbated albuminuria and increased mesangial expansion and glomerular fibrosis in diabetic

207 ic changes such as arteriolar hyalinosis and mesangial expansion are common, however, determining eti

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

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

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

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

212 Mesangial expansion underlies diabetic nephropathy, lead

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

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

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

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

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

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

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

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

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

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

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

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

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

226 nterstitial fibrosis, arteriolar hyalinosis, mesangial expansion, etc.) were similar in prevalence an

227 -777 decreased proteinuria, podocyte injury, mesangial expansion, fibrosis, and CD68 macrophage infil

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

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

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

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

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

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

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

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

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

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

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

239 p, glomerular basement membrane (GBM) width, mesangial fractional volume, and ACR increased, and surf

240 ntly associated with increases in GBM width, mesangial fractional volume, and mean glomerular volume,

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

242 ephritis with typical abnormalities, such as mesangial hypercellularity and immune complex deposition

243 defects, including expanded capillary lumen, mesangial hypercellularity, synechiae formation, and pod

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

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

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

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

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

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

250 Most mesangial IgA1 in human IgAN has a hypogalactosylated hi

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

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

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

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

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

256 e during the regenerative phase after severe mesangial injury.

257 area in the glomerular tufts increased after mesangial injury.

258 rular regeneration after murine experimental mesangial injury.

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

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

261 Deletion of COX-2 from the interstitial/mesangial lineage displayed a less severe phenotype than

262 reases in albuminuria, urinary H(2)O(2), and mesangial matrix accumulation in db/db mice and fully pr

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

264 Mesangial matrix accumulation is an early feature of glo

265 dation, and increased levels of albuminuria, mesangial matrix accumulation, and urinary H(2)O(2) Admi

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

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

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

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

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

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

272 notype classifications highly correlate with mesangial matrix expansion scored by a pathologist (R.E.

273 Albuminuria, mesangial matrix expansion, and glomerular hypertrophy w

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

275 ssive renal pathologies, including fibrosis, mesangial matrix expansion, and tubular hypertrophy were

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

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

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

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

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

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

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

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

284 ature embraced by podocytes and supported by mesangial myofibroblasts, which ensure plasma filtration

285 Early mesangial nephritis initiates a cascade of inflammatory

286 Mesangial pathology is widely acknowledged to reflect gl

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

288 We show mesangial processes invading the capillary loops of both

289 d TrkC-OE mice exhibited enlarged glomeruli, mesangial proliferation, basement membrane thickening, a

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

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

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

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

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

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

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

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

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

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

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