ライフサイエンスコーパス: mesangial cell

1 localization demonstrated Nox5 expression in mesangial cells.

2 aled SGPL1 expression in mouse podocytes and mesangial cells.

3 brotic proteins in both proximal tubular and mesangial cells.

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

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

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

7 matory cytokine expression in rat glomerular mesangial cells.

8 calized inflammatory responses by activating mesangial cells.

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

10 1 is activated by TGF-beta1 in primary mouse mesangial cells.

11 genase increased AT1R expression in cultured mesangial cells.

12 stimulation of type I collagen expression in mesangial cells.

13 TAK1 activation in response to TGF-beta1 in mesangial cells.

14 F-beta receptors type I and type II in renal mesangial cells.

15 ing activation and proliferation of PECs and mesangial cells.

16 , to excessive ROS production by alpha1-null mesangial cells.

17 the expression of lipocalin-2 in glomerular mesangial cells.

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

19 ceptor (EGFR) phosphorylation in alpha1-null mesangial cells.

20 he development and maintenance of glomerular mesangial cells.

21 sively within the glomerular endothelial and mesangial cells.

22 ) B chain or PDGF receptor (PDGFR) beta lack mesangial cells.

23 y of collagen IV to interact with glomerular mesangial cells.

24 ailed to direct sufficient GATA3 activity to mesangial cells.

25 t attenuated TGF-beta-induced hypertrophy of mesangial cells.

26 on induced by the 5-HT(2A) receptor in renal mesangial cells.

27 seen in both mouse embryonic fibroblasts and mesangial cells.

28 omplex formation in glomerular podocytes and mesangial cells.

29 -beta1 promotes the PIP complex formation in mesangial cells.

30 and longer term increases in DNA content in mesangial cells.

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

32 ation was explored in vitro using glomerular mesangial cells.

33 duced profibrogenic responses in primary rat mesangial cells.

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

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

36 glucose-induced matrix production by kidney mesangial cells.

37 mmatory responses and proliferation of human mesangial cells.

38 In human mesangial cells (a microvascular pericyte that secretes

39 merular extracellular matrix deposition, and mesangial cell activation in TSLPtg mice.

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

41 re detected in the glomerulus and glomerular mesangial cells after tail vein injection in normal and

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

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

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

45 miR302 overexpressing mesangial cells also exhibited enhanced expression of EZ

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

47 chidonic acid can enhance AT1R expression in mesangial cells and augment the profibrotic effects of a

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

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

50 EB phosphorylation in HKC-8 cells but not in mesangial cells and fibroblasts.

51 ridization showed expression of TLR4 mRNA in mesangial cells and glomerular epithelial cells.

52 he AT2 receptor, were significantly lower in mesangial cells and glomeruli derived from 12/15-lipoxyg

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

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

55 ithelial cells (HKC-8) but not in glomerular mesangial cells and interstitial fibroblasts.

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

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

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

59 Mesangial cells and podocytes express integrins alpha1be

60 receptor Fn14, and that TWEAK stimulation of mesangial cells and podocytes induces a potent proinflam

61 In cultured mesangial cells and proximal tubule cells, where both PP

62 Mesangial cells and their matrix form the central stalk

63 pe I and transforming growth factor-beta1 in mesangial cells and to be highly expressed during tubulo

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

65 that kidney beta8 is localized to glomerular mesangial cells, and expression is decreased in mouse mo

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

67 roscopy demonstrated that endothelial cells, mesangial cells, and podocytes of immature glomeruli syn

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

69 xpressed in renal arterial smooth muscle and mesangial cells, and tubules around adult vasa rectae ex

70 In cultured human mesangial cells, angiostatin blocked the overexpression

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

72 Glomerular mesangial cells are active participants in the pathogene

73 effects of these factors on endothelial and mesangial cells are also discussed.

74 of metanephric mesenchymal cells, from which mesangial cells are derived.

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

76 Renal mesangial cells are responsible for glomerular PAF gener

77 Mesangial cells are specialized pericyte/smooth muscle c

78 irculating hemopoietic cells, rather than on mesangial cells, are required for IC-mediated pathogenes

79 itful area of future research is the role of mesangial cells as local modulators of innate and adapti

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

81 However, in kidney mesangial cells, as opposed to podocytes, encephalomyoca

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

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

84 Mesangial cell attachment to collagen I led to increased

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

86 anine glomerular isolates and cultured human mesangial cells but lacked similar effects in vascular c

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

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

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

90 hage-conditioned medium (MPCM)-injured human mesangial cells can be modulated by this receptor.

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

92 and fibronectin (FN) in AT1R-overexpressing mesangial cells compared with control cells.

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

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

95 ression of glucose transporter 1 (GLUT-1) in mesangial cells could induce a "diabetic cellular phenot

96 ue plasminogen activator protein detected in mesangial cell culture supernatants without affecting th

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

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

99 Mesangial cells cultured under high glucose conditions p

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

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

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

103 starved, growth-arrested, near confluent rat mesangial cell cultures were stimulated to divide in med

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

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

106 f TWEAK on kidney cells were confirmed using mesangial cells derived from Fn14-deficient mice and by

107 rray gene profiling was performed in primary mesangial cells (derived from lupus-prone MRL/lpr mice)

108 osis, suggesting that beta8 regulates normal mesangial cell differentiation.

109 Our results revealed that cultured primary mesangial cells displayed a concentration-dependent incr

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

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

112 The cytokines generated by mesangial cells, endothelial cells, and podocytes that t

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

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

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

116 nes were comparable to those found following mesangial cell exposure to potent proinflammatory stimul

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

118 We found that murine mesangial cells express cell surface TWEAK receptor.

119 Mesangial cells expressing Hic-5 showed altered latent T

120 Mesangial cell expression of the LIM protein hydrogen pe

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

122 Mesangial cells, found in the glomerulus of the kidney,

123 Similarly, cultured mesangial cells from alpha1-null mice showed elevated ex

124 expression levels of all three MMPs, whereas mesangial cells from Alport mice show elevated expressio

125 In contrast, elevated MMP-9 levels in mesangial cells from Alport mice were linked to ERK path

126 ated MMP-2, -9, and -14 expression levels in mesangial cells from integrin alpha1-null mice.

127 Mesangial cells from itgb8-/- mice backcrossed to a gene

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

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

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

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

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

133 Glomerular mesangial cell (GMC) proliferation and matrix expansion

134 ession also has been described in glomerular mesangial cells (GMC), where COX-2 is not expressed cons

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

136 ma receptors or using Fcgamma chain-knockout mesangial cells had no effect on the gene regulation eff

137 Whether mesangial cells have a distinct origin from vascular smo

138 Integrin alpha1-null mesangial cells have constitutively increased basal leve

139 Mesangial cell Hic-5 expression was associated with incr

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

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

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

143 thelin-1 (ET-1) stimulation of primary human mesangial cells (HMCs) induces betaPix and p66Shc up-reg

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

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

146 0, resulting in the inhibition of mTORC1 and mesangial cell hypertrophy and fibronectin and PAI-1 exp

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

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

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

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

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

152 ssion of PTEN inhibited high-glucose-induced mesangial cell hypertrophy, and expression of dominant-n

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

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

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

156 Mesangial cells in kidney glomeruli were also significan

157 ing hemopoietic cells and of kidney resident mesangial cells in pathogenesis, (NZB x NZW)F1 bone marr

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

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

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

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

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

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

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

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

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

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

168 ression of CCN2/CTGF in human lung and renal mesangial cells is inhibited by 10 nm PGE(2), whereas hu

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

170 In both glomeruli and cultured mesangial cells isolated from integrin alpha1-null mice,

171 TWEAK stimulation of mesangial cells led to a dose-dependent increase in CCL2

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

173 rlying the induction of MC collagen, a mouse mesangial cell line MES-13 was employed.

174 Mesangial cell lysates from ACE-I-treated cells were abl

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

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

177 iabetic nephropathy (DN) is characterized by mesangial cell (MC) expansion and accumulation of extrac

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

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

180 extracellular matrix genes, is increased in mesangial cells (MC) in DN.

181 Contractility of mesangial cells (MC) is tightly controlled by [Ca(2+)](i

182 Overexpression of AGER1 in murine mesangial cells (MCs) (MC-R1) inhibited AGE-induced MAPK

183 ANG II activates mesangial cells (MCs) and stimulates the synthesis of ex

184 Mesangial cells (MCs) are essential for normal renal fun

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

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

187 n Ab showed enhanced binding to immortalized mesangial cells (MCs) derived from a lupus prone MRL-lpr

188 Mesangial cells (MCs) from CE(2) mice maintained their e

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

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

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

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

193 st, expression of glomerular endothelial and mesangial cell miRNAs (miR-126 and miR-145, respectively

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

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

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

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

198 ACE-I induced an increase in mesangial cell MMP9 mRNA, but reduced the MMP9 enzyme ac

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

200 h muscle actin assembly, which characterizes mesangial cell myofibroblast transformation in renal dis

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

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

203 We conclude that the beta8 cytosolic tail in mesangial cells organizes a signaling complex that culmi

204 ced an increase in LRP surface expression in mesangial cells over that in control cells and that this

205 In renal mesangial cells, overexpression of FXR or treatment with

206 Mesangial cell PAI-1 and MCP-1 mRNA expression were upre

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

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

209 Mouse mesangial cells plated on MGO-modified collagen IV showe

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

211 despite persistent expression of FcRgamma in mesangial cell populations.

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

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

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

215 e the mechanism whereby integrin alpha1-null mesangial cells produce excessive ROS.

216 Wild-type but not TLR2-deficient mesangial cells produced CXC chemokines in response to s

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

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

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

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

221 Endothelin-1 promotes mesangial cell proliferation and sclerosis.

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

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

224 PGN with massive glomerular immune deposits, mesangial cell proliferation, extensive mesangial matrix

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

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

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

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

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

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

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

232 Thus, mesangial cell research still holds much promise.

233 Mesangial cell responses were then examined in the two s

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

235 TWEAK stimulation of mesangial cells resulted in an increase in phosphorylate

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

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

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

239 Mesangial cells showed matrix expansion, increased colla

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

241 Cultured mesangial cells showed reduced migratory potential when

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

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

244 In human glomerular mesangial cells, Smad3 protein levels were specifically

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

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

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

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

249 reduced the MMP9 enzyme activity detected in mesangial cell supernatants.

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

251 However, lack of known unique mesangial cell surface markers has hampered this process

252 how that ACE-I treatment is able to modulate mesangial cell-surface expression of LRP, providing an a

253 injury by inhibiting apoptosis and promoting mesangial cell survival.

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

255 provides endothelial cytoprotection against mesangial cell TGF-beta.

256 49F-renal fibroblasts (but not in tubular or mesangial cells) TGF-beta similarly activates PAK2 as we

257 Mesangial cells that were derived from WKY rats synthesi

258 Mesangial cells that were isolated from S/Pla mice had a

259 directly modulate gene expression in kidney mesangial cells through both Fc-dependent and non-Fc-dep

260 Similarly, exposure of mesangial cells to high concentrations of glucose also d

261 Here, we exposed cultured human and mouse mesangial cells to high glucose and transforming growth

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

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

264 We conclude that TWEAK induces mesangial cells to secrete proinflammatory chemokines, s

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

266 n, whereas decreased beta8 activation shifts mesangial cells toward a RhoA-dependent myofibroblast ph

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

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

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

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

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

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

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

274 egrin expressed on the surface of glomerular mesangial cells was selected as a target molecule for de

275 In cultured rat mesangial cells, we found that the 12/15-lipoxygenase pr

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

277 ls could contribute to disease exacerbation, mesangial cells were cultured and found to express mRNA

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

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

280 may contribute toward disease exacerbation, mesangial cells were studied and shown to express TLR2 a

281 oA-associated myofibroblast differentiation, mesangial cells were transduced with inhibitory Rac pept

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

283 -beta1-induced type I collagen expression in mesangial cells, whereas knock down of BAT3 protein expr

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

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

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

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

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

289 ently inhibits PDGF-induced DNA synthesis in mesangial cells with an IC(50) of 10 microM without indu

290 receptor-associated protein to MPCM-injured mesangial cells with and without ACE-I increased the amo

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

292 Transient transfection of murine mesangial cells with iNOS promoter deletion-luciferase c

293 stimulation of wild-type and TLR4-deficient mesangial cells with LPS caused production of CXC chemok

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

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

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

297 eta significantly reduced PTEN expression in mesangial cells, with a reduction in its phosphatase act

298 or cells as epithelial cells (podocytes) and mesangial cells within the damaged glomerulus, leading t

299 and IL-6 by TNF-alpha-or IL-1beta-stimulated mesangial cells without any effect on cell viability or

300 , targeted delivery of therapeutic agents to mesangial cells would be an attractive approach to treat