ライフサイエンスコーパス: tubular epithelial cell

1 by stimulating apoptosis in endothelial and tubular epithelial cell.

2 e expressed in nuclei of proximal and distal tubular epithelial cells.

3 n-induced apoptosis of immortalized proximal tubular epithelial cells.

4 d larval survival and proliferation of renal tubular epithelial cells.

5 tection with persisting reduced apoptosis of tubular epithelial cells.

6 and sonic hedgehog ligands) are expressed in tubular epithelial cells.

7 appaB/NF-kappaB activation in human proximal tubular epithelial cells.

8 B-mediated cyclooxygenase-2 (COX-2) in renal tubular epithelial cells.

9 membrane transporters on the luminal side of tubular epithelial cells.

10 BK polyomavirus in primary cultures of renal tubular epithelial cells.

11 ass transmembrane protein expressed in renal tubular epithelial cells.

12 the effect of complement on the phenotype of tubular epithelial cells.

13 a redox-dependent activation of Akt in renal tubular epithelial cells.

14 xidized lipoproteins, expressed by apoptotic tubular epithelial cells.

15 e actin and expression of S100A4 in proximal tubular epithelial cells.

16 s well as a microfluorimetry study of kidney tubular epithelial cells.

17 Nase I and EndoG mediate cisplatin injury to tubular epithelial cells.

18 ction of laminin-beta1 synthesis in proximal tubular epithelial cells.

19 plex with ILK at the focal adhesion sites of tubular epithelial cells.

20 nd RelB, which were predominantly located in tubular epithelial cells.

21 y and downregulated E-cadherin expression in tubular epithelial cells.

22 is followed by regeneration of damaged renal tubular epithelial cells.

23 regenerating tubules are derived from renal tubular epithelial cells.

24 aspase 3 expression, present mostly on renal tubular epithelial cells.

25 gainst the in vitro hypoxia injury of kidney tubular epithelial cells.

26 cing factor (AIF) in cisplatin-treated renal tubular epithelial cells.

27 specifically and permanently in mature renal tubular epithelial cells.

28 n synthesis and induces hypertrophy in renal tubular epithelial cells.

29 ity in the kidney and cultured primary renal tubular epithelial cells.

30 time- and dose-dependent manner in proximal tubular epithelial cells.

31 he expression of inhibitory Smad-6 and -7 in tubular epithelial cells.

32 not in Smad3-deficient, primary mouse kidney tubular epithelial cells.

33 viral antigen ICC predominantly involved the tubular epithelial cells.

34 nflammatory action, likely via NF-kappaB, on tubular epithelial cells.

35 expression of SODD on the luminal surface of tubular epithelial cells.

36 ng on glomerular endothelial cells and renal tubular epithelial cells.

37 posed at least in part of degenerating renal tubular epithelial cells.

38 enchymal cells such as hepatocytes and renal tubular epithelial cells.

39 , pre-, and pri-miR-214 than normal proximal tubular epithelial cells.

40 hi homologue 1 (Msi1), which is expressed in tubular epithelial cells.

41 titutively expressed by human renal proximal tubular epithelial cells.

42 ed in proximity to the polyomavirus-infected tubular epithelial cells.

43 uced alterations in these levels in proximal tubular epithelial cells.

44 the sustained in-vivo modification of renal tubular epithelial cells.

45 A induced Nupr1 expression in cultured human tubular epithelial cells.

46 in primary neuronal cells and renal proximal tubular epithelial cells.

47 expression, and internalization within renal tubular epithelial cells.

48 d an enrichment of miR-24 in endothelial and tubular epithelial cells.

49 and by inhibiting bacteria invasion of renal tubular epithelial cells.

50 t decrease in proliferation and apoptosis of tubular epithelial cells.

51 o reduced bacterial internalization by renal tubular epithelial cells.

52 ous functional parameters in endothelial and tubular epithelial cells.

53 ansmembrane TNF-alpha in cultured CD4- renal tubular epithelial cells, 293T cells, and HeLa cells ena

54 In transfected tubular epithelial cells, 4-PBA did not improve maturati

55 beta-catenin, predominantly in podocytes and tubular epithelial cells, accompanied renal injury; pari

56 c miR-24 enrichment in renal endothelial and tubular epithelial cells after I/R induction.

57 can contribute to the regeneration of renal tubular epithelial cells after I/R injury.

58 nd downstream Src activation both in primary tubular epithelial cells after in vitro stimulation with

59 ound to be induced rapidly in human proximal tubular epithelial cells after TGF-beta1 treatment.

60 results suggest that netrin-1 protects renal tubular epithelial cells against ischemia reperfusion-in

61 wever, Mif gene deletion restricted to renal tubular epithelial cells aggravated these effects.

62 pses between HIV-harboring T cells and renal tubular epithelial cells, allowing viral uptake and gene

63 overexpression of DNase I in cultured mouse tubular epithelial cells also induced EndoG.

64 along endothelial cells and inside proximal tubular epithelial cells also.

65 nuria caused a decrease in the proportion of tubular epithelial cells and an increase in the proporti

66 7-deficient mice exhibited less apoptosis of tubular epithelial cells and better renal function than

67 t natural killer (NK) cells are cytotoxic to tubular epithelial cells and contribute to acute kidney

68 this death receptor is up-regulated in renal tubular epithelial cells and endothelial cells of some i

69 important because it typically damages renal tubular epithelial cells and glomerular cells and is the

70 e kidneys was observed primarily in cortical tubular epithelial cells and in correlation with the pro

71 uction of proinflammatory mediators by renal tubular epithelial cells and inflammatory cells (eg, mon

72 atory responses through acting on both renal tubular epithelial cells and inflammatory cells and by i

73 CYP3A5 protein expression was detected in tubular epithelial cells and inflammatory cells within t

74 MP-activated protein kinase (AMPK) in kidney tubular epithelial cells and interstitial fibroblasts.

75 duced inflammatory mediators from both renal tubular epithelial cells and macrophages after hypoxia/r

76 at Dragon may enhance BMP signaling in renal tubular epithelial cells and maintain normal renal physi

77 l of TGF-beta1-induced EMT by BMP-7 in renal tubular epithelial cells and mammary ductal epithelial c

78 and p21 expression in human kidney 2 (HK-2) tubular epithelial cells and normal rat kidney-49 fibrob

79 ted with fluorescently tagged HIV with renal tubular epithelial cells and observed efficient virus tr

80 TMIGD1 is expressed in renal tubular epithelial cells and promotes cell survival.

81 bules occurs primarily from proliferation of tubular epithelial cells and resident renal-specific ste

82 ventually replacing the irreversibly injured tubular epithelial cells and restoring tubular integrity

83 ecovery and repair involves proliferation of tubular epithelial cells and stem cell populations and t

84 d multicellular tubulogenesis in mouse renal tubular epithelial cells and that these morphogenic effe

85 to TrkA phosphorylation in mesangial cells, tubular epithelial cells, and podocytes but not in glome

86 activate transforming growth factor-beta1 in tubular epithelial cells, and this process occurred in a

87 ice developed mesangial matrix expansion and tubular epithelial cell apoptosis in association with in

88 s and macrophages, chemokine expression, and tubular epithelial cell apoptosis in kidney.

89 l cycle dysregulation and apoptosis of renal tubular epithelial cells are important components of the

90 Proximal tubular epithelial cells are major sites of homocysteine

91 Despite that tubular epithelial cells are the major sites of active v

92 f epithelial-mesenchymal transition, whereby tubular epithelial cells are transformed into activated

93 1 expression in response to TGF-beta1 in rat tubular epithelial cells as well as in mouse fibroblasts

94 proliferating cell nuclear antigen-positive tubular epithelial cells at 24 hours after the ischemia-

95 These findings demonstrate that tubular epithelial cells at the perimeter of the macula

96 During proteinuria, renal tubular epithelial cells become exposed to ultrafiltrate

97 In tubular epithelial cells, both norepinephrine and CGRP i

98 tin expression in TSC2(+/-) primary proximal tubular epithelial cells; both inhibition of Akt and inh

99 Both demonstrated TGF-beta1 in tubular epithelial cells, but Sir was associated with pr

100 ates tight junction-associated activities in tubular epithelial cells, but the function of DbpA in me

101 nin-beta1 synthesis in murine renal proximal tubular epithelial cells by 30 mmol/l glucose (high gluc

102 Damage to renal tubular epithelial cells by genetic, environmental, or b

103 trix protein laminin-beta1 in renal proximal tubular epithelial cells by stimulation of initiation ph

104 Under pathologic conditions, renal tubular epithelial cells can undergo epithelial to mesen

105 VHL led to dysplastic hyperproliferation of tubular epithelial cells, confirming the procarcinogenic

106 reated with unilateral renal IRI, persistent tubular epithelial cell damage was determined in the IRI

107 -1R(+) or CD68(+)) that induced apoptosis of tubular epithelial cells, damaging the kidney.

108 ntin, which can activate NK cells to mediate tubular epithelial cell death in vitro, was highly expre

109 rized by uncontrolled renal inflammation and tubular epithelial cell death.

110 In renal tubular epithelial cells, decreased Smad3 levels were ob

111 from ischemia/reperfusion injury, surviving tubular epithelial cells dedifferentiate and proliferate

112 Ca(2+) ion channels, respectively, result in tubular epithelial cell-derived renal cysts.

113 Mice lacking Cdc42 specifically in kidney tubular epithelial cells died of renal failure within we

114 However, podocytes and renal tubular epithelial cells do not express CD4 receptors, a

115 wn of SnoN expression by RNA interference in tubular epithelial cells dramatically sensitized their r

116 sed expression of 6-O-sulfated HS domains in tubular epithelial cells during chronic rejection as com

117 olves numerous different cell types, such as tubular epithelial cells, endothelial cells, and podocyt

118 suppression of UNC5B expression in cultured tubular epithelial cells exacerbated cisplatin-induced c

119 ion, whereas IL-22 receptor was expressed by tubular epithelial cells exclusively.

120 Tubular epithelial cells exposed to serum proteins adopt

121 Nearly all renal tubular epithelial cells express insulin receptor.

122 Tubular epithelial cells expressed IL-15 constitutively,

123 induced tubulointerstitial injury, with some tubular epithelial cells expressing alpha-smooth muscle

124 Tubular epithelial cell expression of SPI-6 blocks granz

125 Studies have shown that podocytes and renal tubular epithelial cells from patients with HIV-associat

126 astructure of fibroblasts and renal proximal tubular epithelial cells from patients with three clinic

127 ression of PSF-TFE3 in normal renal proximal tubular epithelial cells from where such tumors originat

128 core role for miR-192 in mediating proximal tubular epithelial cell G2/M arrest after toxic injury b

129 served increased apoptosis in renal proximal tubular epithelial cells, greater expression of LC3-II/L

130 In addition, Nlrp3KO tubular epithelial cells had an increased repair respons

131 In a separate arm, renal tubular epithelial cells (HK-2) were directly stimulated

132 Human proximal tubular epithelial cells (HK-2) were examined after incu

133 In cultured human kidney tubular epithelial cells (HK-2), TGF-beta1 treatment ind

134 an hepatic epithelial cells (L-02) and human tubular epithelial cells (HK-2).

135 Human proximal tubular epithelial cells (HK2 cells) undergo EMT in resp

136 agen catabolizing activity of human proximal tubular epithelial cells (HKC) that were treated with TG

137 Alu-containing (SnoN) expression in proximal tubular epithelial cells (HKC-8) but not in glomerular m

138 -1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8).

139 acid are linked to growth arrest of proximal tubular epithelial cells; however, the underlying mechan

140 We show that primary human proximal tubular epithelial cells (HPTECs) possess characteristic

141 kidneys or oxidant stress in human proximal tubular epithelial cells (HPTECs), KIM-1 expression incr

142 s BKV entry pathways in human renal proximal tubular epithelial cells (HRPTEC) and, correspondently,

143 Since human renal proximal tubular epithelial cells (HRPTEC) represent a main natur

144 ithelial cells (HiBEC), human renal proximal tubular epithelial cells, human bronchial epithelial cel

145 ling pathways, mediates Ang II-induced renal tubular epithelial cell hypertrophy.

146 TGF-beta1 induced ILK expression in renal tubular epithelial cells in a time- and dose-dependent m

147 RNA and protein expression in human proximal tubular epithelial cells in a time-dependent fashion, an

148 Mature tubular epithelial cells in adult kidney can undergo epi

149 und that Nod1 and Nod2 were present in renal tubular epithelial cells in both mouse and human kidneys

150 VEGF-positive cells were observed mainly in tubular epithelial cells in CO-treated, but not air-expo

151 e tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes, mediated in part b

152 The proliferation of mouse proximal tubular epithelial cells in ex vivo culture depends on m

153 in-like protein that is upregulated in renal tubular epithelial cells in HIVAN.

154 gnificantly decreased frequency of apoptotic tubular epithelial cells in IFNAR-deficient mice, as com

155 VEGFA is also expressed in tubular epithelial cells in kidney; however, its physiol

156 Renal tubular epithelial cells in S-phase were scored as femal

157 ular elongation and shape maintenance of two tubular epithelial cells in the C. elegans excretory sys

158 ized predominantly to the apical surfaces of tubular epithelial cells in the thick ascending limbs, d

159 is by using Madin-Darby Canine Kidney (MDCK) tubular epithelial cells in two- or three-dimensional (2

160 adhesion molecules, CD44 and annexin II, in tubular epithelial cells in vitro and in vivo, and treat

161 is also expressed by primary renal proximal tubular epithelial cells in vitro as demonstrated by FAC

162 re, inhibition of Crry expressed by proximal tubular epithelial cells in vitro resulted in alternativ

163 In human proximal tubular epithelial cells in vitro, PAR2 stimulation with

164 toxic effects on renal endothelial cells and tubular epithelial cells in vitro.

165 n the extracellular compartment) in proximal tubular epithelial cells in vivo.

166 -7 leads to repair of severely damaged renal tubular epithelial cells, in association with reversal o

167 many epithelial cell types, including renal tubular epithelial cells, in which they are felt to part

168 nduce marked morphogenic actions in cultured tubular epithelial cells, including scattering, migratio

169 catenin in the cytoplasm and nuclei of renal tubular epithelial cells, indicating activation of the c

170 Tubular epithelial cells induce significant CD8+ T-cell

171 Tubular epithelial cell-induced CD8 degranulation and CD

172 plasmin (20 microg/ml) to cultures of murine tubular epithelial cells initiated ERK phosphorylation w

173 Meprin A plays an important role in tubular epithelial cell injury during acute kidney injur

174 or of obstruction-induced renal fibrosis and tubular epithelial cell injury independent of TGF-beta1

175 affected patients are secondary to extensive tubular epithelial cell injury induced by the lytic repl

176 uch growth arrest to fibrosis after proximal tubular epithelial cell injury, this mechanism may have

177 tigen was detected in less than 5% of VSMCs, tubular epithelial cells, interstitial endothelium, inte

178 Oxidative damage to renal tubular epithelial cells is a fundamental pathogenic mec

179 elatively unknown, despite that apoptosis of tubular epithelial cells is commonly observed in human r

180 The dysfunction and apoptosis/necrosis of tubular epithelial cells is of key importance for the pa

181 complex, localizes to primary cilia of renal tubular epithelial cells, is required for ciliogenesis,

182 In vitro, primary renal tubular epithelial cells isolated from KO animals were r

183 uring kidney morphogenesis and repair, renal tubular epithelial cells lacking the transmembrane recep

184 In human renal tubular epithelial cell line (HK-2), VAN induced p53 acc

185 line (LLC-EZ) using the pig kidney proximal tubular epithelial cell line (LLC-PK1), which constituti

186 n microarray studies that used a novel renal tubular epithelial cell line from a patient with HIVAN,

187 result of oxidative stress; in the proximal tubular epithelial cell line HK-2, TINag expression and

188 yzed this region in the human renal proximal tubular epithelial cell line HK-2.

189 and characterized in LLC-PK1 cells, a renal tubular epithelial cell line with proximal tubule charac

190 In MDCK, a kidney tubular epithelial cell line, cells, low concentrations

191 tol, and xylitol in a porcine renal proximal tubular epithelial cell line, LLC-PK1.

192 study conducted on the human renal proximal tubular epithelial cell line, RPTEC/TERT1, treated with

193 mation was studied in vitro using a proximal tubular epithelial cell line.

194 ablished conditionally immortalized proximal-tubular epithelial cell lines (ciPTECs) from three patie

195 tors in cisplatin-induced apoptosis in renal tubular epithelial cells (LLC-PK1).

196 macula densa, the observation was made that tubular epithelial cells located near the macula densa a

197 tated NLRP3 inflammasome activation in renal tubular epithelial cells, macrophages, and dendritic cel

198 etween inflammatory infiltrates and resident tubular epithelial cells may play important roles in the

199 receptor on the surface of injured proximal tubular epithelial cells, mediating phagocytosis of apop

200 he expression of clusterin in renal proximal tubular epithelial cells obtained from patients with nep

201 reased expression of IL-36alpha in the renal tubular epithelial cells of a mouse model of unilateral

202 Apoptosis was also detected in the tubular epithelial cells of CP-treated mice using immuno

203 iopoietin-2 expression markedly increased in tubular epithelial cells of fibrotic kidneys but decreas

204 be overexpressed in the proximal and distal tubular epithelial cells of murine and human kidneys aft

205 nstrated that these factors are expressed in tubular epithelial cells of postischemic kidneys.

206 es, BK virus (BKV) replication occurs in the tubular epithelial cells of the kidney, causing nephropa

207 a low level of regenerative competence, the tubular epithelial cells of the nephrons can proliferate

208 d that the absence of C3aR and C5aR on renal tubular epithelial cells or circulating leukocytes atten

209 BMDC contributed to the renal tubular epithelial cell population, although most (90%)

210 During kidney organogenesis, tubular epithelial cells proliferate until a functional

211 or-independent mechanism to facilitate renal tubular epithelial cell proliferation and renal tubular

212 he intracellular mechanisms underlying renal tubular epithelial cell proliferation and tubular repair

213 n of plasma creatinine correlating with less tubular epithelial cell proliferation compared to the yo

214 Increased tubular epithelial cell proliferation is a prerequisite

215 Similar reductions in renal tubular epithelial cell proliferation were observed foll

216 either globally or conditionally in proximal tubular epithelial cells, protected mice from the develo

217 al tubular epithelial cellcaused by proximal tubular epithelial cell (PTC) apoptosis.

218 s and determine its effect on renal proximal tubular epithelial cell (PTC) function, because this is

219 phenotypic modulation of the renal proximal tubular epithelial cell (PTC).

220 dy, the effect of high glucose on a proximal tubular epithelial cell (PTEC) line was investigated.

221 Factor H dose-dependently bound to proximal tubular epithelial cells (PTEC) in vitro.

222 rotic target cells by viable kidney proximal tubular epithelial cells (PTEC) modulates the activity o

223 Proximal tubular epithelial cells (PTEC) not only constitute a ma

224 Impaired albumin reabsorption by proximal tubular epithelial cells (PTECs) has been highlighted in

225 Mouse proximal tubular epithelial cells (PTECs) in culture were then ex

226 totic target cells by viable kidney proximal tubular epithelial cells (PTECs) inhibits the proliferat

227 ial-mesenchymal transition (EMT) of proximal tubular epithelial cells (PTECs) into myofibroblasts con

228 Yet, the responses of proximal tubular epithelial cells (PTECs) to fluid flow remain un

229 Injury of proximal tubular epithelial cells rapidly and strongly induced Nu

230 We used human renal proximal tubular epithelial cells, rat kidney transplants, and HO

231 In addition to tubular epithelial cells, recent studies indicate that e

232 of endogenous AGS3 mRNA and protein in renal tubular epithelial cells reduced cell proliferation in v

233 In this study, we found that dying tubular epithelial cells released histones into the extr

234 otein 13 (TRIP13) is a critical modulator of tubular epithelial cell repair following ischemia-reperf

235 ous SnoN or Ski after transfection conferred tubular epithelial cell resistance to TGF-beta1-induced

236 nd Hmox1 in centrilobular hepatocytes and in tubular epithelial cells, respectively.

237 ssue-specific inactivation of KIF3A in renal tubular epithelial cells results in viable offspring wit

238 ate proinflammatory events in renal proximal tubular epithelial cells (RPTEC) via interaction with CD

239 Dysregulated apoptosis of renal tubular epithelial cells (RTEC) is an important componen

240 Here, using renal tubular epithelial cells (RTECs) derived from FAT10(-/-)

241 We hypothesized that renal tubular epithelial cells (RTECs) isolated from hibernati

242 Both glomerular and tubular epithelial cells showed enhanced expression of p

243 Studies in kidney-proximal tubular epithelial cells showed that SNP abrogated high

244 Notably, tubular epithelial cell-specific overexpression of IL-17

245 monstrate successful transgene expression in tubular epithelial cells, specifically in the S(3) segme

246 In human proximal tubular epithelial cells, stimulation by fluvoxamine or

247 and EMT through the NF-kappaB pathway in the tubular epithelial cells, suggesting a novel role for th

248 Renal tubular epithelial cells synthesize laminin (LN)5 during

249 accumulation, activation, and Mphi-mediated tubular epithelial cell (TEC) apoptosis during unilatera

250 h subclinical rejection, suggesting that the tubular epithelial cell (TEC) expression of this protein

251 Clear cell renal cell carcinoma (ccRCC), a tubular epithelial cell (TEC) malignancy, frequently sec

252 chemic renal injury is often reversible, and tubular epithelial cell (TEC) proliferation is a hallmar

253 s significantly upregulated (1 to 3-fold) by tubular epithelial cells (TEC) and infiltrating mononucl

254 ed that miR-21 is expressed in proliferating tubular epithelial cells (TEC) and up-regulated by both

255 TNFR) superfamily, is induced in human renal tubular epithelial cells (TEC) in response to injury.

256 Previous studies revealed that tubular epithelial cells (TEC) show a limited response t

257 tor (CSF)-1 and its receptor CSF-1R on renal tubular epithelial cells (TEC) will promote proliferatio

258 IL-34 was generated by tubular epithelial cells (TECs) and promoted Mo-mediated

259 To elucidate the mechanisms by which renal tubular epithelial cells (TECs) control the complement s

260 ation, and activation, is upregulated in the tubular epithelial cells (TECs) during kidney inflammati

261 ceptor superfamily, is up-regulated in human tubular epithelial cells (TECs) during renal injury, but

262 show that activation of the Notch pathway in tubular epithelial cells (TECs) in patients and in mouse

263 NK) cell-mediated cytotoxicity against renal tubular epithelial cells (TECs) plays a crucial role dur

264 We hypothesize that human renal tubular epithelial cells (TECs) trigger selective prolif

265 NLRP3 expression in renal tubular epithelial cells (TECs) was found to be an impor

266 pithelial-to-mesenchymal transition (EMT) of tubular epithelial cells (TECs).

267 In proximal tubular epithelial cells, TGF-beta1 treatment causes a d

268 VTEA enabled us to discover a population of tubular epithelial cells that expresses CD11C, a marker

269 Snail1 reactivation induces a partial EMT in tubular epithelial cells that, without directly contribu

270 Here macrophages, growth-arrested tubular epithelial cells, the endothelium, and surroundi

271 t, FBP1 antagonizes glycolytic flux in renal tubular epithelial cells, the presumptive ccRCC cell of

272 sitive cells relative to interstitial space, tubular epithelial cells, the tubular basement membrane

273 -1 also increased albumin uptake by proximal tubular epithelial cells through the PI3K and ERK pathwa

274 Exposure of renal proximal tubular epithelial cells to 10 mum cadmium demonstrated

275 Exposure of proximal tubular epithelial cells to high glucose causes a rapid

276 Exposure of proximal tubular epithelial cells to high glucose contributes to

277 beta1 integrin was required for renal tubular epithelial cells to mediate GDNF- and FGF-depend

278 IP13 increased the susceptibility of damaged tubular epithelial cells to progress towards apoptotic c

279 ogressive tubulointerstitial fibrosis, renal tubular epithelial cells transform into alpha-smooth mus

280 In vascular smooth muscle cells and renal tubular epithelial cells, treatment with thrombospondin-

281 d alpha-particle irradiation-induced loss of tubular epithelial cells triggers a chain of adaptive ch

282 th muscle actin and fibronectin induction in tubular epithelial cells, underscoring its ability to bl

283 reteral obstruction model of renal fibrosis, tubular epithelial cells upregulated the chemokine CXCL1

284 ial fibroblasts are actually originated from tubular epithelial cells via EMT in diseased kidney.

285 st that IL-18 induces profibrotic changes in tubular epithelial cells via increased TLR4 expression/s

286 acid led to profound G2/M arrest in proximal tubular epithelial cells via p53-mediated inactivation o

287 etion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 defi

288 rivascular and periglomerular regions, while tubular epithelial cells were alpha-SMA-negative.

289 TAM expression and shedding by tubular epithelial cells were investigated by PCR and en

290 situ hybridization for tTg mRNA showed that tubular epithelial cells were the major source of tTg; h

291 To test the role of HO-1, renal proximal tubular epithelial cells were treated with HO-1 small in

292 Primary mouse tubular epithelial cells were treated with methylglyoxal

293 many epithelial cell types, including renal tubular epithelial cells, where they participate in flow

294 ssion and activity at 24 h in renal proximal tubular epithelial cells, which was inhibited by sodium

295 e infected immortalized and primary proximal tubular epithelial cells with adenovirus to express eith

296 in type 1 diabetes and treatment of proximal tubular epithelial cells with high glucose leads to phos

297 with these findings, treating human proximal tubular epithelial cells with PAR2-AP induced Smad2/3 ph

298 of vascular smooth muscle cells (VSMCs) and tubular epithelial cells, with a median positivity of 20

299 ptor type 1 (TbetaR1) kinase specifically in tubular epithelial cells, with expression restricted by

300 nduced a biphasic activation of ILK in renal tubular epithelial cells, with rapid activation starting