ライフサイエンスコーパス: tubular cell

1 tered tubular cells arise from any surviving tubular cell.

2 s or whether recovery involves any surviving tubular cell.

3 otection required both macrophages and renal tubular cells.

4 ork for nutrient transport in renal proximal tubular cells.

5 absorption of the protein tracer in proximal tubular cells.

6 caused by ischemic or toxic injury to renal tubular cells.

7 xpression was mainly limited to the proximal tubular cells.

8 tro alternative activation of macrophages by tubular cells.

9 that recovery from AKI occurs from intrinsic tubular cells.

10 1alpha-hydroxylase in immortalized proximal tubular cells.

11 nd attenuated the expression of cyclin B1 in tubular cells.

12 d fibrosis that is highly expressed in renal tubular cells.

13 uce apoptosis or regulated necrosis of renal tubular cells.

14 iapoptotic effect of ouabain in Stx2-exposed tubular cells.

15 es of transgenic albumin and IgG in proximal tubular cells.

16 hilic 2OGAs can specifically target proximal tubular cells.

17 receptor Axl in the apical membrane of renal tubular cells.

18 ent epithelial cells, fibroblasts and kidney tubular cells.

19 ys leading to apoptosis or survival in renal tubular cells.

20 nchymal transition induced by FGF-2 in renal tubular cells.

21 partment favoring the FGF-2-dependent EMT of tubular cells.

22 ouse inner medullary collecting duct-3 renal tubular cells.

23 ivation of HIF target genes only in proximal tubular cells.

24 came apparent later in both interstitial and tubular cells.

25 of M2 macrophages when cocultured with renal tubular cells.

26 t4, thereby inhibiting de-differentiation of tubular cells.

27 al sodium channel alpha, ENaCalpha, in renal tubular cells.

28 induced autophagy in cultured renal proximal tubular cells.

29 itical role in TGF-beta-induced EMT of renal tubular cells.

30 ed by knocking out Tsc1 in a subset of renal tubular cells.

31 ts Vpr-induced apoptosis in human and murine tubular cells.

32 dependent inflammatory mediators in proximal tubular cells.

33 induced ACE2 down-regulation in human kidney tubular cells.

34 lpha (2)-glycoprotein (Zag) in aged proximal tubular cells.

35 e-induced mitochondrial dysfunction in renal tubular cells.

36 -1, RANTES, and CXCL10 as MAP3K14 targets in tubular cells.

37 ligand 8 (CXCL8)/CXCL1 expression by injured tubular cells.

38 rofibrotic effect in cultured renal proximal tubular cells.

39 albumin-induced profibrotic effects in renal tubular cells.

40 demonstrated high levels of CtsD in damaged tubular cells.

41 of ECVs derived from glomerular and proximal tubular cells.

42 tion of NF-kappaB in cultured renal proximal tubular cells.

43 and dramatically enhanced in PPARalpha(-/-) tubular cells.

44 or detecting ER stress in podocytes or renal tubular cells.

45 arly survival mechanisms in severely damaged tubular cells.

46 amin, and was selective for ECVs from kidney tubular cells.

47 inclusions of monoclonal LC within proximal tubular cells.

48 glomeruli including podocytes and in distal tubular cells.

49 upregulated MANF expression in podocytes and tubular cells.

50 mechanotransducers, particularly in proximal tubular cells.

51 that angiotensin II can activate SREBP-1 in tubular cells.

52 tive mapping of polymyxin in kidney proximal tubular cells.

53 ntly expressed in podocytes but not in renal tubular cells.

54 1 knockout (Ddah1(PT-/-)) mouse demonstrated tubular cell accumulation of ADMA and lower NO concentra

55 G2/M-arrested proximal tubular cells activate c-jun NH(2)-terminal kinase (JNK)

56 endogenous Foxc2 in the cytoplasm of injured tubular cells activates epithelial cell redifferentiatio

57 D receptor (VDR) and p65 formed a complex in tubular cells after paricalcitol treatment, which inhibi

58 t3 transcription factor has been reported in tubular cells after renal damage, and Stat3 has been imp

59 ed characteristics of all segments of kidney tubular cells and cultured KSP+ cells in 3D Matrigel, wh

60 nimals by promoting proliferation of injured tubular cells and decreasing apoptosis, but whether thes

61 How proximal tubular cells and distal professional proton transportin

62 In the kidneys of diabetic mice, apoptotic tubular cells and dysmorphic mitochondria were observed,

63 es including the vascular endothelium, renal tubular cells and erythrocytes.

64 Whereas murine renal tubular cells and freshly isolated renal tubules rapidly

65 modeling using cultured human proximal renal tubular cells and half-nephrectomized mice treated with

66 atin accumulates preferentially in the renal tubular cells and is a frequent cause of drug-induced AK

67 is a glycoprotein released by damaged renal tubular cells and is a sensitive maker of both clinical

68 In vitro, necrotic tubular cells and oxidative stress induced IL-22 secreti

69 analysis revealed Pals1 expression in renal tubular cells and podocytes of human kidneys.

70 Microarrays of proximal tubular cells and podocytes with stable HIF1alpha and/or

71 including the capacity to differentiate into tubular cells and podocytes, as demonstrated by confocal

72 d increased profibrotic proteins in proximal tubular cells and podocytes; a miR-150 inhibitor reverse

73 the significant uptake of polymyxin in renal tubular cells and provides crucial information for the u

74 may cause mitochondrial dysfunction in renal tubular cells and reprogramming of glucose metabolism.

75 orrelated with higher proliferative rates of tubular cells and significantly fewer senescent cells.

76 Vpr induces increased expression of FAT10 in tubular cells and that inhibition of FAT10 expression pr

77 ischemia/reperfusion in sublethally injured tubular cells and that the protein is located in the cyt

78 endoplasmic reticulum (ER) stress in kidney tubular cells and the expression of RTN1A correlates wit

79 eins shows a predominant expression in renal tubular cells and the localization of immunoreactive Fgb

80 y to the recovering outer medullary proximal tubular cells and was highly coexpressed with Ki-67, a m

81 LLC-PK1 tubular cells and whole kidneys from C57BL/6 mice were s

82 ation in distal tubular rather than proximal tubular cells and/or nontubular cells mediates protectiv

83 ry of ATP, reduced apoptosis and necrosis of tubular cells, and abrogated tubular dysfunction.

84 pon reperfusion is essential for survival of tubular cells, and inhibition of oxidative damage can li

85 expression of angiogenic factors in proximal tubular cells, and it may ameliorate renovascular hypert

86 aused a marked concentrating defect, loss of tubular cells, and slowly progressive renal fibrosis.

87 Mif deletion also resulted in reduced tubular cell apoptosis after UUO.

88 Notably, both tubular cell apoptosis and acute kidney injury were atte

89 age (CS) of donor kidneys is associated with tubular cell apoptosis and caspase-3 activation.

90 hemic acute kidney injury through regulating tubular cell apoptosis and inflammation suggesting PTEN

91 VD) induces ischemic injury characterized by tubular cell apoptosis and interstitial fibrosis.

92 ficient to cause AKI characterized by marked tubular cell apoptosis and necrosis, oxidative stress, d

93 e poststenotic kidney may be responsible for tubular cell apoptosis and renal dysfunction but can be

94 d Bak from proximal tubules attenuated renal tubular cell apoptosis and suppressed renal interstitial

95 n vitro, miR-26a inhibition induced proximal tubular cell apoptosis and upregulated proapoptotic prot

96 PTEN inhibition enhanced tubular cell apoptosis in kidneys with IRI, which was as

97 Tubular cell apoptosis seemed frequent in the few studie

98 Simultaneous acute tubular necrosis and tubular cell apoptosis was rare (55 animals [32.4%]) and

99 The prevalence of tubular cell apoptosis was significantly higher in studi

100 nd BcL-xL, and substantially exacerbation of tubular cell apoptosis were inversely correlated with mi

101 exhibited increased initial tubular injury, tubular cell apoptosis, and serum creatinine after ische

102 rosis, independent of NOX2, through enhanced tubular cell apoptosis, decreased microvascularization,

103 ies (170 animals) assessed the prevalence of tubular cell apoptosis, which was reported in 158 animal

104 uld protect against caspase-3 activation and tubular cell apoptosis.

105 associated with loss of XIAP and subsequent tubular cell apoptosis.

106 and is associated with significantly reduced tubular cell apoptosis.

107 I was characterized by marked renal proximal tubular cell apoptosis.

108 tion, with increased kidney injury and renal tubular cell apoptosis.

109 his reparative response that serves to limit tubular cell apoptotic death via activation of Akt, impr

110 n in sepsis but presents focally; most renal tubular cells appear normal.

111 To resolve whether scattered tubular cells are fixed progenitors, cells were irrevers

112 eviously shown that 13-lined ground squirrel tubular cells are protected from apoptotic cell death du

113 Myofibroblasts produced from EMT of renal tubular cells are responsible for the deposition of extr

114 sed significantly, indicating that scattered tubular cells arise from any surviving tubular cell.

115 interactions between filtered endotoxin and tubular cells as a possible mechanism of AKI in sepsis.

116 d accelerated the proliferation of surviving tubular cells as early as 1 day after reperfusion.

117 lved in the circadian clock system, in renal tubular cells (Bmal1(lox/lox)/Pax8-rtTA/LC1 mice).

118 renal filter and are reabsorbed by proximal tubular cells, but it is not clear whether the endocytos

119 sis and abolished proliferation in wild-type tubular cells, but only reduced proliferation in Nupr1-d

120 plays an essential role in the EMT of renal tubular cells, but the molecular mechanism governing thi

121 enerative capacity of actively cycling renal tubular cells by decreasing the number of cells in G2/M

122 water and sodium reabsorption via increased tubular cell cAMP levels, we hypothesized the ET would a

123 Taken together, these data show that tubular cells can instruct macrophage activation by secr

124 We have observed that, in renal proximal tubular cells, cardiotonic steroids such as ouabain in v

125 In cultured human tubular cells, cisplatin reduced SIRT3, resulting in mit

126 in vitro studies of cultured tubular cells confirm the cytoplasmic location of Foxc2

127 Renal proximal tubular cells constantly recycle nutrients to ensure min

128 iR-26a on apoptosis was evaluated in a renal tubular cell culture.

129 In LPS-stimulated tubular cell cultures, Mif deletion led to enhanced G2/M

130 Cisplatin induced a higher degree of tubular cell damage and apoptosis in regions where TINag

131 , a reduction in apoptosis and a decrease in tubular cell damage in kidneys with nephrotoxic or IRI i

132 intervention reduced hemolysis-related renal tubular cell damage, hepatocyte damage, ileal leakage of

133 evulinic acid (ALA) accumulates and promotes tubular cell death and tubulointerstitial damage.

134 chondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains l

135 sed histologic injury, oxidative stress, and tubular cell death in this model.

136 procurement for transplantation can lead to tubular cell death via necrosis and apoptosis, which tri

137 ed to donor or recipient decreased the renal tubular cell death, inflammation, and MHC II expression,

138 ted fibrosis, the inflammatory response, and tubular cell death.

139 ical ischemic renal injury by its paucity of tubular cell death.

140 likely unable to inhibit Notch resulting in tubular cell death.

141 istent Cav-EGFR-ERK signaling mediates renal tubular cell dedifferentiation and identifies a novel mo

142 acute tubular necrosis, apoptosis, and renal tubular cell desquamation, with toxic vacuolization and

143 In summary, scattered tubular cells do not represent a fixed progenitor popula

144 ecrosis (necroptosis), which occurs in renal tubular cells during AKI.

145 ependent of parietal epithelial and proximal tubular cell effects has not been possible so far.

146 y MANF excretion concurrent with podocyte or tubular cell ER stress preceded clinical or histologic m

147 t Nox4 protein is robustly induced in kidney tubular cells exclusively by combined application of con

148 acetylation was also noted in mesangial and tubular cells exposed to 25 mmol/L compared with 5.6 mmo

149 However, murine renal cortical and medullary tubular cells expressed Gb(3) and responded to Stx2 by u

150 Both in vitro and after renal I/R, tubular cells expressed GM-CSF, a known STAT5 activator,

151 Macrophages promote the proliferation of tubular cells following ischemic injury, suggesting that

152 -1 (KIM-1) is highly upregulated in proximal tubular cells following kidney injury.

153 Root hairs are single tubular cells formed from the differentiation of epiderm

154 linking FAT1 and RAC1/CDC42 to podocyte and tubular cell function.

155 Furthermore, tubular cells had reduced PGC-1alpha expression and oxyg

156 cally found in the brush borders of proximal tubular cells, has been detected in urine of patients wi

157 effects of fructose in human kidney proximal tubular cells (HK-2) and whether they are mediated by th

158 trated that xenon exposure to human proximal tubular cells (HK-2) led to activation of range of prote

159 TGF-beta-induced EMT of human renal proximal tubular cells (HPTCs).

160 uence of acute kidney injury (AKI), proximal tubular cells hyperrespond to endotoxin (lipopolysacchar

161 Unilateral nephrectomy initiates tubular cell hypertrophy and proliferation in the contra

162 nal cyst formation by suppressing pathologic tubular cell hypertrophy and proliferation.

163 enal vessels and induces hypertension, renal tubular cell hypertrophy, and podocyte apoptosis.

164 ression of membrane sodium channels in renal tubular cells in a manner dependent on the metabolic che

165 stochemistry localized MAP3K14 expression to tubular cells in acute folate nephropathy and human AKI.

166 , modulates redox imbalance and apoptosis in tubular cells in diabetes, but these mechanisms remain u

167 Renal MIF expression was reduced in tubular cells in fibrotic compared with healthy murine a

168 Kidney tubular cells in Glis2-knockout mice acquire mesenchymal

169 ron accumulation on the apical side of renal tubular cells in Heph/Cp KO mice.

170 rial fragmentation also occurred in proximal tubular cells in mice during renal ischemia/reperfusion

171 CtsD expression was upregulated in damaged tubular cells in nephrotoxic and ischemia reperfusion (I

172 r H was present on the urinary side of renal tubular cells in proteinuric, but not in normal renal ti

173 kers for detecting ER stress in podocytes or tubular cells in the incipient stage of disease, when a

174 ects of kaempferol and esculetin using renal tubular cells in vitro and in vivo in a mouse Unilateral

175 Recombinant MIF exerted opposing effects on tubular cells in vitro and in vivo Our data identify ren

176 Prolonged CS of tubular cells in vitro and whole mouse kidneys ex vivo i

177 and type 1 diabetic animals and in proximal tubular cells incubated with normal or high glucose.

178 In allografts with tubular cell infection, epithelial cells of the proximal

179 acute cellular rejection had allografts with tubular cell infection.

180 decline in allograft function compared with tubular cell infection.

181 improved renal and tubular function and less tubular cell inflammation during reperfusion.

182 uggest that activation of PKC-delta promotes tubular cell injury and death during albuminuria, broade

183 bulointerstitial inflammation, fibrosis, and tubular cell injury and death, but the mechanisms underl

184 n, translocated to mitochondria early during tubular cell injury, and both siRNA knockdown of Drp1 an

185 s of fatty acid binding protein, a marker of tubular cell injury, were dramatically reduced by PP but

186 clusions about the direct role of TGFbeta in tubular cell injury.

187 ect of PGI2 on hypoxia/reoxygenation-induced tubular cells injury or I/R kidneys by measuring oxidati

188 Immortalized rat renal proximal tubular cells (IRPTCs) and kidneys from humans with T2D

189 and concentration of polymyxin within renal tubular cells is essential for the development of novel

190 whether the selective activation of Stat3 in tubular cells is involved in the development of intersti

191 In vitro studies using proximal tubular cells isolated from HO-1(-/-) and wild-type kidn

192 Primary proximal tubular cells isolated from IkappaBalphaDeltaN-expressin

193 y cultures treated with cyclosporin A, renal tubular cells isolated from Nupr1-deficient mice exhibit

194 rtTA mouse coexpressed markers for scattered tubular cells (kidney injury molecule 1, annexin A3, src

195 Proximal tubular cells labeled by the PEC-rtTA mouse coexpressed

196 enerated a mouse model in which the proximal tubular cells lack Dicer, a key enzyme for microRNA prod

197 l mononuclear phagocytes and directly damage tubular cells, leading to the release of the NLRP3 agoni

198 and GTPase activating protein in a proximal tubular cell line (HK-2).

199 In a human proximal tubular cell line (HKC-8), paricalcitol inhibited RANTES

200 Here, in a rat kidney proximal tubular cell line (RPTC), albumin induced apoptosis in a

201 ce C3b deposition on a mouse kidney proximal tubular cell line (TEC) and a human retinal pigment epit

202 MP-7 on response to TGF-beta in the proximal tubular cell line HK-2 (PTC).

203 A human kidney tubular cell line in which beta1-integrin was knocked do

204 Also, in a human proximal tubular cell line, cholera toxin or a Rapgef4-specific a

205 ulated expression of IRF-1 in an S3 proximal tubular cell line.

206 TORC1) pathway was downregulated in proximal tubular cell lines derived from Ctns(-/-) mice.

207 Nonspecific changes (vacuolization of tubular cells, loss of brush border, and tubular cell sw

208 In cultured tubular cells, MAP3K14 small interfering RNA targeting d

209 In CKD, tubular cells may be involved in the induction of inters

210 macologic inhibition of STAT5, we found that tubular cell-mediated macrophage alternative activation

211 transporter 2 (PEPT2) expressed by proximal tubular cells mediates the reabsorption of ALA, and vari

212 epletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was observed

213 rats (Han:SPRD Cy/+), demonstrating obvious tubular cell morphological abnormalities.

214 In proximal tubular cells, mRNA levels of the amino acid transporter

215 The ischemically injured kidney undergoes tubular cell necrosis and apoptosis, accompanied by an i

216 l inflammation, neutrophil infiltration, and tubular cell necrosis and improved excretory renal funct

217 nd transient translocation into the proximal tubular cell nuclei.

218 apoptosis, resulting in an increase in total tubular cell numbers.

219 on reduction caused Stat3 phosphorylation in tubular cells of lesion-prone mice but not in resistant

220 Within 15 min of reperfusion, proximal tubular cells of the S3 segment produced IRF-1, which is

221 osis and restored autophagy/mitophagy in the tubular cells of these mice.

222 ept for selective drug targeting of proximal tubular cells on the basis of specific transporters, giv

223 docytes predominately (38% of recipients) or tubular cells only (62% of recipients).

224 Pi transport in primary cultures of proximal tubular cells or in freshly isolated renal tubules revea

225 mouse also efficiently labels the scattered tubular cell population.

226 proliferation (2.6 times decreased), better tubular cell preservation (E-cadherin 14 times increased

227 Here, we exposed proximal tubular cells, primary mesangial cells, and podocytes to

228 Moreover, tubular cell proliferation after ischemia/reperfusion wa

229 Primary cilia dysfunction alters renal tubular cell proliferation and differentiation and assoc

230 depletion at 3 to 5 days after injury slows tubular cell proliferation and repair.

231 Furthermore, MIF inhibition reduced tubular cell proliferation in vitro In all three in vivo

232 The diabetic milieu triggers early tubular cell proliferation, but the induction of TGF-bet

233 eg expansion in spleen and kidney, increased tubular cell proliferation, improved renal function, and

234 reased ciliogenesis in cyst cells, increased tubular cell proliferation, increased apoptosis, increas

235 proinflammatory macrophages, promoted renal tubular cell proliferation.

236 onal reconstructions reveal actin-associated tubular cell protrusions, reminiscent of filopodia, but

237 To test this, we induced proximal tubular cell (PTC) injury in Balb/c mice and Nfatc1(+/-)

238 found that Rab27a was expressed in proximal tubular cells (PTCs) and partially colocalized with the

239 ed expression profiling of cultured proximal tubular cells (PTCs) under high-glucose and control cond

240 s known as a key function of kidney proximal tubular cells (PTCs), to date, no single protease has be

241 tructural and functional changes in proximal tubular cells (PTCs), with focus on endocytosis of ultra

242 regulated proteome in primary human proximal tubular cells (PTEC) to identify potential AngII activit

243 Poor baseline tubular cell quality (defined by a higher rate of tubula

244 candidate proregeneratory factor in primary tubular cell recovery, and IL-22 deficiency or IL-22 blo

245 Knockdown of Fat1 in renal tubular cells reduces migration, decreases active RAC1 a

246 During the development of AKI the quiescent tubular cells reenter the cell cycle.

247 During recovery, the frequency of labeled tubular cells remained constant, arguing against a fixed

248 these intrinsic cells (so-called "scattered tubular cells") represent fixed progenitor cells or whet

249 sD and B were located in distal and proximal tubular cells respectively in human disease.

250 cytes, or neurons), cardiomyocytes or kidney tubular cells respectively.

251 of PIKfyve in endocytically active proximal tubular cells resulted in the development of large cytop

252 primary filtrate and reabsorbed by proximal tubular cells, resulting in serum accumulation.

253 expression, hypertension, and renal proximal tubular cell (RPTC) injury in high-glucose milieu both i

254 pression of catalase (CAT) in renal proximal tubular cells (RPTCs) could prevent the programming of h

255 by reactive oxygen species in renal proximal tubular cells (RPTCs) in models of diabetes.

256 e adapted primary cultures of renal proximal tubular cells (RPTCs) that exhibit in vivo levels of aer

257 ensinogen (AGT) production in renal proximal tubular cells (RPTCs) via inflammatory cytokines, includ

258 contributors to late graft loss; features of tubular cell senescence, such as increased p16(INK4a) ex

259 and prevented TLR-4/NF-kappaB activation in tubular cells; serum pro-inflammatory cytokines IL-1beta

260 itu We now show that EV from adult rat renal tubular cells significantly improved renal function when

261 Furthermore, specific deletion of Stat3 in tubular cells significantly reduced the extent of inters

262 Inducible and tubular cell-specific knockdown of Shroom3 markedly abro

263 e crystal-related acute kidney injury, dying tubular cells stain positive for phosphorylated MLKL.

264 This technique allowed the imaging of tubular cell structure and function with multiphoton mic

265 Tubular cells subjected to prolonged CS in vitro demonst

266 of PPARalpha and increased in PPARalpha(-/-) tubular cells, suggesting that PPARalpha interacts with

267 tubules as a critical determinant of initial tubular cell survival and reparative proliferation after

268 e early stages of kidney repair and promotes tubular cell survival via IL-13 receptor alpha2 (IL13Ral

269 of tubular cells, loss of brush border, and tubular cell swelling) were each observed in 423 (39.9%)

270 In renal tubular cells, TGF-beta1 administration upregulated SHRO

271 ns at a frequency of 63 mHz were observed in tubular cells that were within 100 microm of the macula

272 uria has been shown to injure renal proximal tubular cells, the effects of albumin on podocytes have

273 volved in the physiologic response of kidney tubular cells to DNA damage, which contributes to the pa

274 G5 (two key autophagic genes) sensitized the tubular cells to hypoxia-induced apoptosis.

275 of mesangial cells, podocytes, and proximal tubular cells to propose the development of ORG as a mal

276 tein expression and abolished the ability of tubular cells to recruit lymphocytes and monocytes after

277 vitro, myoglobin treatment induced proximal tubular cells to secrete chemoattractants and macrophage

278 Here, exposing rat proximal tubular cells to Stx2 in vitro resulted in massive apopt

279 However, the molecular mechanisms that link tubular cells to the interstitial compartment are not cl

280 In cultured tubular cells, transient transfection with a miR-324-3p

281 bstructive nephropathy and in PPARalpha(-/-) tubular cells treated with Wnt3a.

282 en might be a sign of recurring increases of tubular cell turnover that potentially provide enhanced

283 , NOX4 is crucial for the survival of kidney tubular cells under injurious conditions.

284 e that can be adopted by almost any proximal tubular cell upon injury.

285 The PEC-rtTA mouse labeled more tubular cells upon different tubular injuries but was in

286 HIF-2alpha activation in renal tubular cells upregulated mRNA and protein expressions o

287 likely to play multiple roles in regulating tubular cell viability, repair, and remodeling in the ma

288 anion transporters (OATs) in renal proximal tubular cells, we hypothesized that hydrophilic 2OGAs ca

289 single rat (NRK-52E) and human (HK-2) kidney tubular cells were approximately 1930- to 4760-fold high

290 Mitochondria in proximal tubular cells were particularly sensitive to damage in d

291 dney lesions because CHOP-deficient proximal tubular cells were resistant to ER stress-induced cell d

292 motif) ligand 5 (CXCL5) expression in kidney tubular cells, which recruits destructive neutrophils th

293 e ACE and down-regulate ACE2 in human kidney tubular cells, which were blocked by an angiotensin II (

294 Furthermore, 87% of proximal tubular cells with activated mechanistic target of rapam

295 Treatment of tubular cells with dasatinib reduced the expression of C

296 as concentrated along the apical membrane of tubular cells with ET but not PA, and urine aquaporin 2

297 Culturing renal proximal tubular cells with free fatty acid and FXR agonists show

298 As with tubular cells with HIF-2alpha activation, those under hy

299 In vitro stimulation of human tubular cells with HMGB1, in a TLR4-dependent system, co

300 cell cycle pathways was seen in murine renal tubular cells with NOTCH overexpression, and molecular s