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 rofibrotic effect in cultured renal proximal tubular cells.

4 albumin-induced profibrotic effects in renal tubular cells.

5 demonstrated high levels of CtsD in damaged tubular cells.

6 of ECVs derived from glomerular and proximal tubular cells.

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

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

9 arly survival mechanisms in severely damaged tubular cells.

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

11 inclusions of monoclonal LC within proximal tubular cells.

12 glomeruli including podocytes and in distal tubular cells.

13 upregulated MANF expression in podocytes and tubular cells.

14 mechanotransducers, particularly in proximal tubular cells.

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

16 tive mapping of polymyxin in kidney proximal tubular cells.

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

18 absorption of the protein tracer in proximal tubular cells.

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

20 xpression was mainly limited to the proximal tubular cells.

21 tro alternative activation of macrophages by tubular cells.

22 that recovery from AKI occurs from intrinsic tubular cells.

23 1alpha-hydroxylase in immortalized proximal tubular cells.

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

25 uce apoptosis or regulated necrosis of renal tubular cells.

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

27 ormations and crystal deposition in proximal tubular cells.

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

29 hilic 2OGAs can specifically target proximal tubular cells.

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

31 ent epithelial cells, fibroblasts and kidney tubular cells.

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

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

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

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

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

37 came apparent later in both interstitial and tubular cells.

38 trophy and fibrosis in kidney glomerular and tubular cells.

39 e tubular cells, while Osx is known to label tubular cells.

40 the transcytosis of dimeric IgA in cultured tubular cells.

41 tegral part of the injury phenotype of renal tubular cells.

42 in vitro using coculture of macrophages and tubular cells.

43 um glucose transporter 2 (SGLT2) in proximal tubular cells.

44 otection required both macrophages and renal tubular cells.

45 nd CXCL10 in polycystic kidneys and cultured tubular cells.

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

47 ork for nutrient transport in renal proximal tubular cells.

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

49 -1, RANTES, and CXCL10 as MAP3K14 targets in tubular cells.

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

51 1 knockout (Ddah1(PT-/-)) mouse demonstrated tubular cell accumulation of ADMA and lower NO concentra

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

53 ng therapeutic strategy for protecting renal tubular cells against cisplatin-induced AKI by enhancing

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

55 e of cystine accumulating in kidney proximal tubular cells and cystine's role in disease progression

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

57 How proximal tubular cells and distal professional proton transportin

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

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

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

61 rtant role in the cross-talk between injured tubular cells and infiltrating immune cells and myofibro

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

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

64 pe I interferon (IFN)-response signatures in tubular cells and keratinocytes distinguished patients w

65 Primary tubular cells and macrophages from SerpinB2 knockout and

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

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

68 vitro, SCFAs modulated inflammation in renal tubular cells and podocytes under hyperglycemic conditio

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

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

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

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

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

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

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

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

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

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

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

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

81 use embryonic fibroblasts and renal proximal tubular cells, and renal ischemia-reperfusion to induce

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

83 ough the glomerulus, is taken up by proximal tubular cells, and transferred to lysosomes.

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

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

86 I group demonstrated significantly increased tubular cell apoptosis and caspase-9 expression, whereas

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

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

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

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

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

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

93 In contrast, the CI+Txp group had tubular cell apoptosis associated with expression of cas

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

95 Tubular cell apoptosis seemed frequent in the few studie

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

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

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

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

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

101 s showed improved renal function by reducing tubular cell apoptosis, pro-inflammatory cytokine expres

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

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

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

105 and is associated with significantly reduced tubular cell apoptosis.

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

107 h emphasis on swan-neck lesions and proximal-tubular-cell apoptosis and proliferation (turnover); and

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

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

110 In mice treated with SS1P, proximal tubular cells are damaged and albumin in the urine is in

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

112 e reciprocal interactions between immune and tubular cells are not well characterized.

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

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 ation is likely required for lithium-induced tubular cell autophagy and protection in cisplatin-induc

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

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

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

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

124 Renal proximal tubular cells constantly recycle nutrients to ensure min

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

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

127 ith its receptor, integrin-beta1, to inhibit tubular cell cycle arrest and apoptosis in in vivo and i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Mouse proximal tubular cells exposed to high glucose showed significant

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

147 s and proliferation (turnover); and proximal-tubular-cell expression of the major apical transporters

148 -1 (KIM-1) is highly upregulated in proximal tubular cells following kidney injury.

149 Analysis of tubular cells from patients with proliferative, membrano

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

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

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

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

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

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

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

157 jury model, and primary cultures of isolated tubular cells in a hypoxia-reoxygenation model.

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

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

160 associated with a beneficial effect on renal tubular cells in AKI.

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

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

163 Kidney tubular cells in Glis2-knockout mice acquire mesenchymal

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

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

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

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

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

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

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

171 Consistently, in cisplatin-injured renal tubular cells in vitro, lithium enhanced autophagic acti

172 tochondrial function, we used human proximal tubular cells in vitro.

173 to reduce phosphate uptake in human proximal tubular cells in vitro.

174 In this process, tubular cells, in coordination with macrophages, overgre

175 CLDN-2 silencing in LLC-PK(1) tubular cells induced activation and phosphorylation of

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

177 acute cellular rejection had allografts with tubular cell infection.

178 decline in allograft function compared with tubular cell infection.

179 the pathways involved in the development of tubular cell injury and death before and after transplan

180 AKI or tubular cell injury was evaluated, and cell signaling as

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

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

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

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

185 ir RPTCs and immortalized rat renal proximal tubular cells (IRPTCs) were also studied.

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

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

188 ty for autophagy in both podocytes and renal tubular cells is markedly impaired in type 2 diabetes, a

189 Primary proximal tubular cells isolated from IkappaBalphaDeltaN-expressin

190 ivation in proximal tubule cells and primary tubular cells isolated from injured kidneys in vitro.

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

192 Primary proximal tubular cells isolated from the knockout mice displayed

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

194 Cultured senescent tubular cells, kidneys of aged mice, and renal stress mo

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

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

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

198 agliflozin on ER stress in the HK-2 proximal tubular cell line and in the kidney of db/db mice to cha

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

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

201 ltures of cilia-deficient or STAT3-deficient tubular cell lines.

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

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

204 ts that were positive for Villin, a proximal tubular cell marker.

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

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

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

208 04 significantly reduced proteinuria-induced tubular cell mitochondrial damage, suggesting that impro

209 the possibility that focusing on normalizing tubular cell mitochondrial function and energy balance c

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

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

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

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

214 n of floxed megalin/LRP2 alleles in proximal tubular cells of cystinotic mice was achieved by a Cre-L

215 ctin-1 (Gal-1), which is highly expressed in tubular cells of kidneys of type 1 and type 2 diabetic m

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

217 e kidney followed by degradation in proximal tubular cells of the kidney.

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

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

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

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

222 mouse also efficiently labels the scattered tubular cell population.

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

224 Moreover, tubular cell proliferation after ischemia/reperfusion wa

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

226 at 1 h and peaked at 12 h after IRI, whereas tubular cell proliferation peaked at 3 d.

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

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

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

230 proinflammatory macrophages, promoted renal tubular cell proliferation.

231 hese results suggest that DsbA-L in proximal tubular cells promotes TIF via activation of the Hsp90 /

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

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

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

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

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

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

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

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

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

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

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

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

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

245 kinase 1 (ASK1) activation in glomerular and tubular cells resulting from oxidative stress may drive

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

247 odifying factor (Bmf)-induced renal proximal tubular cell (RPTC) apoptosis and loss in diabetic mice.

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

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

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

251 bonucleoprotein F (Hnrnpf) in renal proximal tubular cells (RPTCs) suppresses angiotensinogen (Agt) e

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

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

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

255 SerpinB2 knockout tubular cells showed significantly reduced expression of

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

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

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

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

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

261 Tubular cells subjected to prolonged CS in vitro demonst

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

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

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

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

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

267 jor role in the crosstalk between immune and tubular cells that shapes disease expression.

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

269 ors might modulate glucose influx into renal tubular cells, thereby regulating the metabolic conditio

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

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

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

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

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

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

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

277 In cultured murine proximal tubular cells, treatment with PCI34051 or specific HDAC8

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

279 lesions were largely prevented and proximal-tubular-cell turnover was normalized.

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

281 Following insult, the kidney tubular cells undergo a cascade of cellular responses th

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

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

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

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

286 ins could be a source of cystine in proximal tubular cells, we used a mouse model of cystinosis in wh

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

288 In addition, primary tubular cells were cultured to study the function and re

289 response signature and fibrotic signature in tubular cells were each associated with failure to respo

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

291 acrophage colony-stimulating factor by renal tubular cells, which directly stimulates expression of m

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

293 othelial cells, or proximal or loop of Henle tubular cells, while Osx is known to label tubular cells

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

295 bumin induced features of ER stress in renal tubular cells with ATF3/ATF4 activation.

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

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

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

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

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