ライフサイエンスコーパス: mesangial cell

1 mmatory responses and proliferation of human mesangial cells.

2 i that were composed mainly of 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 flammatory SMAD7 and IkappaBalpha factors in mesangial cells.

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

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

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

19 sively within the glomerular endothelial and mesangial cells.

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

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

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

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

24 localization demonstrated Nox5 expression in mesangial cells.

25 aled SGPL1 expression in mouse podocytes and mesangial cells.

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

27 ing activation and proliferation of PECs and mesangial cells.

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

29 he development and maintenance of glomerular mesangial cells.

30 ailed to direct sufficient GATA3 activity to mesangial cells.

31 seen in both mouse embryonic fibroblasts and mesangial cells.

32 ne kinase expressed abundantly in glomerular mesangial cells.

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

34 ation was explored in vitro using glomerular mesangial cells.

35 duced profibrogenic responses in primary rat mesangial cells.

36 complex proteins reduced binding to cultured mesangial cells.

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

38 glucose-induced matrix production by kidney mesangial cells.

39 mTORC1 activation downstream of PDGFRbeta in mesangial cells.

40 In human mesangial cells (a microvascular pericyte that secretes

41 In mesangial cells, ACL is synergistically induced by high

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

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

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

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

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

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

48 miR302 overexpressing mesangial cells also exhibited enhanced expression of EZ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Mesangial cells and podocytes express integrins alpha1be

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

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

66 Mesangial cells and their matrix form the central stalk

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

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

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

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

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

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

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

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

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

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

77 Glomerular mesangial cells are active participants in the pathogene

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

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

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

81 Renal mesangial cells are responsible for glomerular PAF gener

82 Mesangial cells are specialized pericyte/smooth muscle c

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

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

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

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

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

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

89 Mesangial cell attachment to collagen I led to increased

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 Mesangial cells cultured under high glucose conditions p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 Mesangial cells expressing Hic-5 showed altered latent T

125 Mesangial cell expression of the LIM protein hydrogen pe

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

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

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

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

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

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

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

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

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

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

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

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

138 Glomerular mesangial cell (GMC) proliferation and matrix expansion

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

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

141 Whether mesangial cells have a distinct origin from vascular smo

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

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

144 Mesangial cell Hic-5 expression was associated with incr

145 In mesangial cells, high glucose decreased the acetylation

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

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

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

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

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

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

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

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

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

155 0, resulting in the inhibition of mTORC1 and mesangial cell hypertrophy and fibronectin and PAI-1 exp

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

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

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

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

160 kinase deacetylation in high glucose-induced mesangial cell hypertrophy and matrix protein expression

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

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

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

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

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

166 Mesangial cells in kidney glomeruli were also significan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 Endothelin-1 promotes mesangial cell proliferation and sclerosis.

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

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

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

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

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

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

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

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

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

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

236 Thus, mesangial cell research still holds much promise.

237 Mesangial cell responses were then examined in the two s

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

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

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

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

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

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

244 Cultured mesangial cells showed reduced migratory potential when

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

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

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

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

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

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

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

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

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

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

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

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

257 injury by inhibiting apoptosis and promoting mesangial cell survival.

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

259 provides endothelial cytoprotection against mesangial cell TGF-beta.

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

261 Mesangial cells that were derived from WKY rats synthesi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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