ライフサイエンスコーパス: cholangiocyte

1 membrane of biliary epithelial cells (i.e., cholangiocytes).

2 ng process affects the response to injury of cholangiocytes.

3 atoblasts give rise to adult hepatocytes and cholangiocytes.

4 kines and influences epithelial integrity of cholangiocytes.

5 increased RhoU/Wrch1 and Hey2 expression in cholangiocytes.

6 with wild-type RRV, with reduced binding in cholangiocytes.

7 GHS-R1a mRNA was expressed predominantly in cholangiocytes.

8 sive diseases whose primary cell targets are cholangiocytes.

9 rfering RNAs reduced RRV's ability to infect cholangiocytes.

10 ffect on activated fibroblasts and senescent cholangiocytes.

11 Bcl-xL was also up-regulated in senescent cholangiocytes.

12 ent nucleoli, and markers of hepatocytes and cholangiocytes.

13 ne (PBS) before collecting serum, liver, and cholangiocytes.

14 oncogene homolog (NRAS) is activated in PSC cholangiocytes.

15 cinoma cell lines compared with normal human cholangiocytes.

16 duce inflammatory reactions in control large cholangiocytes.

17 vival factor in ASFs as well as in senescent cholangiocytes.

18 virus had reduced binding and infectivity in cholangiocytes.

19 nd in vitro using transwell experiments with cholangiocytes.

20 eins compared to EV released by normal human cholangiocytes.

21 vitro in normal and siRNA-Nlrp3 knocked-down cholangiocytes.

22 receptor, is linked to cAMP and expressed in cholangiocytes.

23 ibition also prevented BSIA in primary mouse cholangiocytes.

24 fibrocystin, a ciliary protein expressed in cholangiocytes.

25 hibit the formation of mesenchymal cells and cholangiocytes.

26 been constrained by a lack of primary human cholangiocytes.

27 an differentiate into mature hepatocytes and cholangiocytes.

28 e increase in hepatocyte progeny relative to cholangiocytes.

29 cholangiocyte (NHC) cells and primary mouse cholangiocytes.

30 ) ligand (CCL)-20 and CCL-2 in human primary cholangiocytes.

31 resone-induced injury in zebrafish and human cholangiocytes.

32 can differentiate into both hepatocytes and cholangiocytes.

33 on was measured by real-time PCR in isolated cholangiocytes.

34 chemokines CCL-20 and CCL-2 in human primary cholangiocytes.

35 d in vitro using trans-well experiments with cholangiocytes.

36 se and alkaline phosphatase were measured in cholangiocytes.

37 biliatresone toxicity in zebrafish and human cholangiocytes.

38 the urothelial cells but inhibited growth of cholangiocytes.

39 ], and TNFSF14 [LIGHT]) produced by reactive cholangiocytes.

40 B to down-regulate ITPR3 expression in human cholangiocytes.

41 generation by restoring both hepatocytes and cholangiocytes.

42 852 resulted in an 80% decrease in senescent cholangiocytes, a reduction of fibrosis-inducing growth

43 tified Twf1 as an important mediator of both cholangiocyte adaptation to aging processes and response

44 ere decreased by approximately 30% in cystic cholangiocytes after treatment with SBI-115 alone and by

45 identify molecular pathways associated with cholangiocyte aging and to determine their effects in th

46 cluding parallel formation of hepatocyte and cholangiocyte anatomical structures.

47 the expression of fibrosis genes in vitro in cholangiocyte and HSC lines.

48 down of MC histidine decarboxylase decreased cholangiocyte and HSC proliferation/activation.

49 Proliferating cholangiocytes and activated hepatic stellate cells (HSC

50 ugh N-terminal, K63-linked ubiquitination in cholangiocytes and activates transcription of a fibrogen

51 ined targeting strategy to deplete senescent cholangiocytes and ASFs from fibrotic tissue to ameliora

52 athies characterized by the damage of mature cholangiocytes and by the appearance of ductular reactio

53 publications of studies of HCV infection of cholangiocytes and CCA cell lines as well as studies of

54 In contrast, in normal deciliated cholangiocytes and CCA cells, the nucleotides induced th

55 /-) livers impairs the biliary commitment of cholangiocytes and enhances the inflammatory reaction an

56 is via the coordinate activation of GalR1 in cholangiocytes and GalR2 in HSCs.

57 itro studies were performed in cell lines of cholangiocytes and hepatic stellate cells (HSCs).

58 ession of AANAT or inhibition of miR-200b in cholangiocytes and hepatic stellate cells decreased the

59 onin synthesis) or inhibition of miR-200b in cholangiocytes and hepatic stellate cells in vitro, we e

60 c progenitor cells (HPCs) differentiate into cholangiocytes and hepatocytes after liver injury.

61 as an emergency cell pool to regenerate both cholangiocytes and hepatocytes and may eventually give r

62 ed HPCs were required for the development of cholangiocytes and hepatocytes in livers after CDE diet-

63 ng the most prominently up-regulated in both cholangiocytes and hepatocytes of biliatresone-treated l

64 5HTR2A/2B/2C and MAO-A/TPH1 are expressed in cholangiocytes and HSCs from BDL rats and Mdr2(-/-) (-)

65 h the receptor subtype (GnRHR1) expressed by cholangiocytes and HSCs.

66 In vitro, cell lines of murine cholangiocytes and human HSCs express 5HTR2A/2B/2C and M

67 sion of TGR5 and Galpha proteins in cultured cholangiocytes and in livers of animal models and humans

68 LB proto-oncogene NF-kappaB subunit in human cholangiocytes and in mouse models of liver disease char

69 protein-coupled receptors expressed by large cholangiocytes and increases large cholangiocyte prolife

70 BTSC differentiation in vitro toward mature cholangiocytes and is associated with PBG activation in

71 biliary cholangitis (PBC) primarily targets cholangiocytes and is characterized by liver fibrosis an

72 rtant for understanding loss of tolerance to cholangiocytes and is relevant to the pathogenesis of se

73 d the effect of subsequent interactions with cholangiocytes and local proinflammatory cytokines on su

74 H69 cholangiocytes and primary mouse cholangiocytes were use

75 MCs are recruited to proliferating cholangiocytes and promote fibrosis.

76 aluated as well as secretion of secretin (by cholangiocytes and S cells), expression of markers of fi

77 Both ductular reactive cholangiocytes and senescent cholangiocytes can modify t

78 -mediated, apoptosis resistance in senescent cholangiocytes and uncovered that ETS1 and the histone a

79 galanin receptor 1 expressed specifically on cholangiocytes and were associated with an activation of

80 rentiate to mature liver cells (hepatocytes, cholangiocytes) and mature pancreatic cells (including f

81 khd1 must be expressed in the target tissue (cholangiocytes) and the immune system (bone marrow).

82 sion was increased both in aged and diseased cholangiocytes, and in human cholangiopathies.

83 lar calcium ion (Ca(2+) ) release channel in cholangiocytes, and its increased expression has been re

84 main intracellular Ca(2+) release channel in cholangiocytes, and loss of it impairs ductular bicarbon

85 er studies revealed a protective role of the cholangiocyte apical glycocalyx, wherein disruption of t

86 logous of CHF, we show that Pkhd1(del4/del4) cholangiocytes are characterized by a beta-catenin-depen

87 Cholangiocytes are the target of a group of chronic live

88 rganoids differentiated into hepatocytes and cholangiocytes, based on the expression of albumin and c

89 The cholangiocyte basolateral side was more vulnerable than

90 During biliary disease, cholangiocytes become activated by various pathological

91 Conclusion: ITPR3 expression in cholangiocytes becomes enhanced in CCA.

92 RL sequence within TRTRVSRLY is required for cholangiocyte binding and viral replication.

93 However, the peptide did not block cholangiocyte binding of TUCH and Ro1845, strains that d

94 ified the amino acid sequence on VP4 and its cholangiocyte binding protein, finding that the sequence

95 ed sensitization to BSIA in AE2-depleted H69 cholangiocytes but even completely prevented BSIA.

96 ical region of endoplasmic reticulum (ER) in cholangiocytes, but both immunogold electron microscopy

97 Evidence of alcohol-induced damage to cholangiocytes, but not ongoing alcohol abuse, affected

98 Human cholangiocytes, but not those with RELB knockdown, proli

99 thelium and exerts its biological effects on cholangiocytes by interaction with the receptor subtype

100 ctular reactive cholangiocytes and senescent cholangiocytes can modify the periductal microenvironmen

101 nded peptides drove proliferation of a human cholangiocyte cell line and demonstrated potent wound he

102 ucinous primary CCA cell cultures, and human cholangiocyte cell lines (H69).

103 Cholangiocyte cell lines and primary cholangiocytes were

104 o the apical and basolateral surfaces of the cholangiocyte channel, allowing proof-of-concept toxicit

105 urvival and increased apoptosis of senescent cholangiocytes, compared to nonsenescent cells.

106 rdinated repopulation of both hepatocyte and cholangiocyte compartment is pivotal to the structure an

107 actin expression in LX-2 cells treated with cholangiocyte-conditioned media.

108 nistered directly to LX-2 cells, but not via cholangiocyte-conditioned media.

109 terized, less is known about whether and how cholangiocytes contribute to this form of cholestasis.

110 or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration by restoring

111 Using cholangiocyte culture and 3D cholangiocyte spheroid cult

112 f HDC protects from HFD-induced fibrosis and cholangiocyte damage.

113 matory responses against large but not small cholangiocyte-derived EVs.

114 n, resulting in the significant emergence of cholangiocyte-derived hepatocytes.

115 ing growth factor beta (TGFbeta) upregulates cholangiocyte-derived signals that activate myofibroblas

116 ways downstream of biliatresone that lead to cholangiocyte destruction and to determine their relatio

117 turally-occurring animal models, that causes cholangiocyte destruction in in-vitro models.

118 COs correspond to mature functional cholangiocytes, differentiating our method from alternat

119 tion and expression of genes associated with cholangiocyte differentiation (cytokeratin 19, connexin

120 Functional cholangiocyte differentiation was demonstrated via incre

121 is required for bile duct morphogenesis and cholangiocyte differentiation.

122 r (SR) axis is up-regulated by proliferating cholangiocytes during cholestasis.

123 and in hepatocyte transdifferentiation into cholangiocytes during liver regeneration to restore bili

124 sone has selective toxicity for extrahepatic cholangiocytes (EHCs) in zebrafish larvae.

125 Human cholangiocytes, epithelial cells lining bile ducts, were

126 This study identifies cholangiocyte EV communication during LPS stimulation, a

127 e for organ regeneration using human primary cholangiocytes expanded in vitro.

128 Here, we show that cholangiocytes express histidine decarboxylase and its i

129 ection, although a subset of hepatocytes and cholangiocytes express the host receptor utilized for ce

130 Cholangiocytes expressed GalR1, whereas HSCs and hepatoc

131 est that PKD1L1 is a biologically plausible, cholangiocyte-expressed candidate gene for the BASM synd

132 Cholangiocyte expression of HSC-activating signals occur

133 and EVs isolated from SCT or SR knocked down cholangiocytes fail to induce inflammatory reactions in

134 previously unidentified early commitment to cholangiocyte fate.

135 ds, which can commit to either hepatocyte or cholangiocyte fates.

136 er expression increased in Twf1 knocked-down cholangiocytes following pro-proliferative and pro-senes

137 y the pathophysiology of the bile duct using cholangiocytes from a variety of sources.

138 Cholangiocytes from DDC-treated mice showed up-regulatio

139 ITPR3 expression was decreased or absent in cholangiocytes from patients with cholestasis of sepsis

140 d for the isolation and propagation of human cholangiocytes from the extrahepatic biliary tree in the

141 eates a "bicarbonate umbrella" that protects cholangiocytes from the proapoptotic effects of bile sal

142 biomarkers and markers of hepatocellular and cholangiocyte function during NEsLP correlate with the d

143 As for cholangiocyte function, bile/perfusate glucose ratio was

144 y biliary markers and mature CLCs displaying cholangiocyte functionality.

145 wever, how relative levels of hepatocyte and cholangiocyte gene expression are determined during diff

146 miR-337-3p stimulates expression of cholangiocyte genes and represses hepatocyte genes in un

147 arge cholangiocytes, respectively, and these cholangiocytes have different morphology and functions.

148 Galanin immunoreactivity was detected in cholangiocytes, hepatic stellate cells (HSCs), and hepat

149 The origin of active cells during DR can be cholangiocytes, hepatocytes, or hepatic progenitor cells

150 NK4a)) expression and senescence in cultured cholangiocytes in an NRAS-dependent manner.

151 The resulting ECOs closely resemble primary cholangiocytes in terms of their transcriptomic profile

152 We showed that mouse cholangiocytes in the channel of the device became polar

153 comparable to ex vivo measurements, and that cholangiocytes in the device were mechanosensitive (as d

154 hat RBPJ promotes HPC differentiation toward cholangiocytes in vitro and blocks hepatocyte differenti

155 ins was increased 2-fold to 3-fold in cystic cholangiocytes in vitro and in vivo.

156 f chemokine (C-C motif) ligand 2 in neonatal cholangiocytes in vitro, and blockade of the correspondi

157 ed cell proliferation via AMPK activation in cholangiocytes in vitro.

158 licate and differentiate into hepatocytes or cholangiocytes in vitro.

159 n conclusion, Nlrp3 is expressed in reactive cholangiocytes, in both murine models and patients with

160 normal urothelium, and H69, established from cholangiocytes, in the presence of S. haematobium or S.

161 We also show that Pkhd1(del4/del4) cholangiocytes, in turn, respond to proinflammatory cyto

162 d EVs induce inflammatory responses in other cholangiocytes including elevated cytokine production an

163 ding proteins enriched at the apical side of cholangiocytes, including CFTR and SLC5A1, as well as re

164 cretin receptor (SR) axis, expressed only by cholangiocytes, increases biliary proliferation, liver f

165 ram-negative bacteria, secrete more EVs than cholangiocytes incubated with vehicle.

166 We present a novel pathway of cholangiocyte injury in a model of biliary atresia, whic

167 nd explore how other stress responses affect cholangiocyte injury in BA.

168 was performed to identify novel modifiers of cholangiocyte injury in the zebrafish experimental BA mo

169 contributing factor in biliatresone-induced cholangiocyte injury, and suggest that variations in int

170 monstrates upregulation of genes involved in cholangiocyte injury/morphology and downregulation of im

171 lestatic injury precedes liver fibrosis, and cholangiocytes interact with HSCs promoting fibrosis.

172 This virus-cholangiocyte interaction is also seen in vivo in the mu

173 isolating and propagating functional primary cholangiocytes is a major limitation in the study of bil

174 pathology, although EV communication between cholangiocytes is not identified to date.

175 ent secretion of growth factors by senescent cholangiocytes leads to the activation of stromal fibrob

176 uripotent stem cells (hPSCs) into functional cholangiocyte-like cells (CLCs).

177 on status of murine LPCs into the progenitor/cholangiocyte lineage while inhibiting hepatocyte differ

178 ol the differentiation of the hepatocyte and cholangiocyte lineages from embryonic liver progenitor c

179 capable of differentiating to hepatocyte and cholangiocyte lineages.

180 of cyclic adenosine monophosphate (cAMP) in cholangiocytes lining liver cysts.

181 notype maintenance, has been associated with cholangiocyte malignant transformation.

182 notype maintenance, has been associated with cholangiocyte malignant transformation.

183 ortantly, expression of mesenchymal cell and cholangiocyte marker was significantly reduced by treatm

184 These BDOs express known cholangiocyte markers including gamma glutamyl transfera

185 and zebrafish has shown that hepatocytes and cholangiocytes may function as facultative stem cells fo

186 The cholangiocyte membrane protein bound by SRL was found to

187 The tripeptide SRL on RRV VP4 binds to the cholangiocyte membrane protein Hsc70, defining a novel b

188 raminidase increased the permeability of the cholangiocyte monolayer after treatment with glycochenod

189 ight junctions, that the permeability of the cholangiocyte monolayer was comparable to ex vivo measur

190 lrp3 knockdown increased the permeability of cholangiocyte monolayers.

191 ITPR3 promoter was measured in normal human cholangiocyte (NHC) cells and primary mouse cholangiocyt

192 accharide-induced senescence in normal human cholangiocytes (NHCs), we found increased BCL-xL mRNA an

193 ly, phospho-ETS1 expression was increased in cholangiocytes of human PSC livers and in the Abcb4 (Mdr

194 L-xL protein expression is increased both in cholangiocytes of livers from individuals with PSC and a

195 rp3 and its components were overexpressed in cholangiocytes of mice subjected to DDC and in patients

196 g protein 3 (Nlrp3) expression was tested in cholangiocytes of normal and cholestatic livers.

197 LDs were also observed in the cholangiocytes of the LivKO mice, but not the floxed con

198 involved in aging processes was evaluated in cholangiocytes of young and old mice (2 months and 22 mo

199 e secretion and subsequently cocultured with cholangiocytes or HSCs prior to measuring fibrosis marke

200 e to differentiate to functional hepatocytes,cholangiocytes or pancreatic islets, yielding similar le

201 eside close to bile ducts and coculture with cholangiocytes or their supernatants induced preferentia

202 naling genetically disrupted in hepatocytes, cholangiocytes, or resident tissue fibroblasts, we have

203 Our platform allows the derivation of cholangiocyte organoids (COs) expressing key biliary mar

204 tic biliary tree in the form of extrahepatic cholangiocyte organoids (ECOs) for regenerative medicine

205 rimary human islets and adult hepatocyte and cholangiocyte organoids.

206 iver injury triggered a ductular reaction of cholangiocyte origin, with approximately 25% of hepatocy

207 secretin receptor (SR), is a key mediator in cholangiocyte pathophysiology.

208 born Jag1(Ndr/Ndr) mice, with aberrations in cholangiocyte polarity, but these defects improved in ad

209 We quantified hepatocyte and cholangiocyte populations in organoids using immunostain

210 of developing hepatocytes and balances both cholangiocyte populations that constitute the ductal pla

211 e acetyltransferases responsible for H3K9ac, cholangiocytes predominantly express Lysine Acetyltransf

212 hypothesis that the chemosensory function of cholangiocyte primary cilia acts as a mechanism for tumo

213 In liver biopsies, disorders of the cholangiocytes primary cilium and various degrees of bil

214 wed by the generation of hepatoblasts (HBs), cholangiocyte progenitors (CPs) expressing early biliary

215 arker Lgr5, and generate both hepatocyte and cholangiocyte progeny that persist for the lifespan of t

216 lestatic liver diseases, mitotically dormant cholangiocytes proliferate and subsequently acquire a ne

217 Cholangiocyte proliferation and ductular reaction contri

218 Galanin treatment increased cholangiocyte proliferation and fibrogenesis in both FVB

219 BDL rats with recombinant galanin increased cholangiocyte proliferation and intrahepatic biliary mas

220 tor 1 (GalR1) and Gal receptor 2 (GalR2), in cholangiocyte proliferation and liver fibrosis in multid

221 demonstrate that Gal contributes not only to cholangiocyte proliferation but also to liver fibrogenes

222 Nlrp3 activation had no effect on cholangiocyte proliferation but significantly decreased

223 uence of interlobular duct remodeling, where cholangiocyte proliferation initially causes corrugation

224 ids using immunostaining and flow cytometry; cholangiocyte proliferation of cholangiocytes was measur

225 hepatic fibrosis in Mdr2KO mice, regulating cholangiocyte proliferation via GHS-R1a, a G-protein cou

226 by large cholangiocytes and increases large cholangiocyte proliferation via histamine-2 receptor (H2

227 Biliary mass and cholangiocyte proliferation were evaluated by immunohist

228 ansport, resulting in cholestasis, increased cholangiocyte proliferation, and intrahepatic cholangioc

229 In vitro, we assessed cholangiocyte proliferation, cAMP levels, and cyst growt

230 -morpholino sequences inhibited hyperplastic cholangiocyte proliferation, liver damage, inflammation,

231 hway and showed that RAGE activation induced cholangiocyte proliferation.

232 of AMPK and FOXO1, maintaining a low rate of cholangiocyte proliferation.

233 ystogenesis by increasing cAMP and enhancing cholangiocyte proliferation; our data suggest that a TGR

234 culture system, we determined that senescent cholangiocytes promoted quiescent mesenchymal cell activ

235 ases termed the "cholangiopathies," in which cholangiocytes react to exogenous and endogenous insults

236 In vitro knockdown of GalR1 in cholangiocytes reduced alpha-smooth muscle actin express

237 Knock-down of Twf1 in cholangiocytes reduced cell proliferation.

238 esults support the conclusion that polarized cholangiocytes release distinct sEV pools to mediate com

239 suggest that ETS1 and p300 promote senescent cholangiocyte resistance to apoptosis by modifying chrom

240 epatic bile ducts consist of small and large cholangiocytes, respectively, and these cholangiocytes h

241 angitis (PSC), the focus of this review, the cholangiocyte response to genetic or environmental insul

242 gated the role of inflammasome activation in cholangiocyte response to injury.

243 Cholangiocytes secrete proinflammatory cytokines during

244 Cholangiocytes secrete stem cell factor, which functions

245 Pharmacologic inhibition or cholangiocyte-selective deletion of Kat2a was protective

246 In vivo, cholangiocyte-selective knockout of EZH2 exacerbates bil

247 molecular mechanisms involved in LPS-induced cholangiocyte senescence and NRAS-dependent regulation o

248 s reveal ETS1 as a central regulator of both cholangiocyte senescence and the associated apoptosis-re

249 We reported that cholangiocyte senescence features prominently in PSC and

250 Cholangiocyte senescence has been linked to primary scle

251 Cholangiocyte senescence is important in PSC pathogenesi

252 Cholangiocyte senescence was assessed by p16(INK4a) in s

253 Cholangiocyte senescence was significantly increased in

254 d histological features of PSC and increased cholangiocyte senescence, a characteristic and potential

255 which blocked CDKN2A expression and reduced cholangiocyte senescence.

256 Large but not small cholangiocytes show inflammatory responses against large

257 r epidermal growth factor receptor (EGFR) in cholangiocyte specification and proliferation, and in he

258 Using cholangiocyte culture and 3D cholangiocyte spheroid cultures, we found that biliatres

259 In CFTR-defective cholangiocytes, Src tyrosine kinase self-activates and p

260 We demonstrate that cholangiocytes stimulated with lipopolysaccharide (LPS),

261 f these reactive proliferative and senescent cholangiocyte subpopulations in PSC.

262 tor-A secretion was measured in serum and/or cholangiocyte supernatant.

263 In vitro, cultured HSCs were stimulated with cholangiocyte supernatants and alpha-smooth muscle actin

264 Stimulation with cholangiocyte supernatants from BDL WT or Kit(W-sh) mice

265 study elucidated how RRV VP4 protein governs cholangiocyte susceptibility to infection both in vitro

266 e 2 (EZH2) as an epigenetic regulator of the cholangiocyte TGF-beta response.

267 y distinct changes in the redox potential of cholangiocytes that differentially sensitized them to bi

268 ation of RELB and increased levels of LTB in cholangiocytes that formed reactive bile ducts compared

269 ed expression of let-7a in BDL and Mdr2(-/-) cholangiocytes that was associated with increased NGF ex

270 Epithelial cells, named cholangiocytes, that line intrahepatic and extrahepatic

271 e limited due to difficulty in accessing the cholangiocyte, the small percentage of these cells in th

272 Cholangiocytes, the epithelial cells lining the biliary

273 ed migration and invasion in normal ciliated cholangiocytes through a P2Y11 receptor and liver kinase

274 E2 in primary biliary cholangitis sensitizes cholangiocytes to apoptotic insults by activating sAC, w

275 mechanism for sensitization of AE2-depleted cholangiocytes to apoptotic stimuli.

276 pathway genes sensitized zebrafish and human cholangiocytes to biliatresone-induced injury independen

277 rc decreased the inflammatory response of CF cholangiocytes to lipopolysaccharide, rescued the juncti

278 own of AE2 sensitized immortalized H69 human cholangiocytes to not only bile salt-induced apoptosis (

279 ive Th17 differentiation in vitro and induce cholangiocytes to produce chemokines mediating recruitme

280 ling intersects with epigenetic machinery in cholangiocytes to support fibrogenic gene transcription.

281 HCs and the otherwise resistant intrahepatic cholangiocytes to the toxin, whereas replenishing GSH le

282 Jag1(+/-) mice without ectopic hepatocyte-to-cholangiocyte transdifferentiation or long-term liver ab

283 o acid change in the RRV VP4 gene influences cholangiocyte tropism and reduces pathogenicity in mice.

284 In cystic cholangiocytes UDCA-HDAC6i #1 restored primary cilium le

285 Finally, BSIA in H69 cholangiocytes was inhibited by intracellular Ca(2+) che

286 ow cytometry; cholangiocyte proliferation of cholangiocytes was measured.

287 Liver tissues and cholangiocytes were collected, and liver damage, changes

288 In the liver of infants with BA, cholangiocytes were found to express IL-17 receptor A, a

289 olipoprotein B and cytochrome P450 activity; cholangiocytes were functional, based on gamma glutamyl

290 Cholangiocytes were isolated from normal human liver, in

291 Second, cholangiocytes were lineage traced with concurrent inhib

292 reporter mice suggested that oval cells and cholangiocytes were the main sources of CTGF and integri

293 H69 cholangiocytes and primary mouse cholangiocytes were used as models.

294 Cholangiocyte cell lines and primary cholangiocytes were used for in vitro studies.

295 large amounts of disease-specific functional cholangiocytes will have broad applications for cholangi

296 Large cholangiocytes with knocked down either SCT or SR by sho

297 We performed RNA sequencing in cholangiocytes with or without TGF-beta.

298 Pretreatment of murine and human cholangiocytes with this VP4-derived peptide (TRTRVSRLY)

299 mplex at the apical membrane of normal mouse cholangiocytes, with proteins that negatively control Ro

300 tions of primary extra- or intrahepatic duct cholangiocytes within 2 weeks of isolation.