ライフサイエンスコーパス: cholangiocyte

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

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

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

4 ibition also prevented BSIA in primary mouse cholangiocytes.

5 fibrocystin, a ciliary protein expressed in cholangiocytes.

6 hibit the formation of mesenchymal cells and cholangiocytes.

7 been constrained by a lack of primary human cholangiocytes.

8 an differentiate into mature hepatocytes and cholangiocytes.

9 e increase in hepatocyte progeny relative to cholangiocytes.

10 cholangiocyte (NHC) cells and primary mouse cholangiocytes.

11 s into mice, which express the cognate Ag on cholangiocytes.

12 olestatic disorders are caused by defects in cholangiocytes.

13 les (EVs) and their internalization by human cholangiocytes.

14 subtypes GnRHR1 and GnRHR2 were expressed in cholangiocytes.

15 ell as proliferation and function markers in cholangiocytes.

16 lls allows production of new hepatocytes and cholangiocytes.

17 t bound NRF2 directly in NHC cells and mouse cholangiocytes.

18 anin blocked EV uptake and IL-6 secretion by cholangiocytes.

19 cells to promote their differentiation into cholangiocytes.

20 ant intracellular calcium release channel in cholangiocytes.

21 kines and influences epithelial integrity of cholangiocytes.

22 chronic inflammatory state of CFTR-defective cholangiocytes.

23 miR-506 expression in vivo in human-diseased cholangiocytes.

24 itis when they recognize the same antigen on cholangiocytes.

25 ntiation is directed towards hepatocytes and cholangiocytes.

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

27 affect senescence and SASP in cultured human cholangiocytes.

28 the biological response to injury by mature cholangiocytes.

29 o myofibroblasts but not into hepatocytes or cholangiocytes.

30 dapted to a lipid-rich diet from bile and/or cholangiocytes.

31 holangiocytes induce senescence in bystander cholangiocytes.

32 , IL-8, CCL2, PAI-1) was also highest in PSC cholangiocytes.

33 arate induced robust and rapid cell death in cholangiocytes.

34 holangiocytes caused senescence in bystander cholangiocytes.

35 -12RB2, and IFN-gamma expressing degenerated cholangiocytes.

36 sive diseases whose primary cell targets are cholangiocytes.

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

38 ffect on activated fibroblasts and senescent cholangiocytes.

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

40 ent nucleoli, and markers of hepatocytes and cholangiocytes.

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

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

43 cinoma cell lines compared with normal human cholangiocytes.

44 duce inflammatory reactions in control large cholangiocytes.

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

46 virus had reduced binding and infectivity in cholangiocytes.

47 eins compared to EV released by normal human cholangiocytes.

48 852 resulted in an 80% decrease in senescent cholangiocytes, a reduction of fibrosis-inducing growth

49 ed the EV proteome and associated changes in cholangiocytes after EV uptake, and we detected EV prote

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

51 cluding parallel formation of hepatocyte and cholangiocyte anatomical structures.

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

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

54 Proliferating cholangiocytes and activated hepatic stellate cells (HSC

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

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

57 l tissue, progenitor cells, hepatocytes, and cholangiocytes and elevated direct bilirubin levels in b

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 cendants are required for the development of cholangiocytes and hepatocytes in liver after CDE diet-i

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

64 ng is observed to occur spontaneously within cholangiocytes and hepatocytes in this model as well as

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

66 e function, as well as histologic markers of cholangiocytes and hepatocytes, were detected in all 3 c

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

68 inducer of senescence, was increased in PSC cholangiocytes and in experimentally induced senescent c

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

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

71 examined interactions between primary human cholangiocytes and isolated intrahepatic T cells ex vivo

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

73 H69 cholangiocytes and primary mouse cholangiocytes were use

74 MCs are recruited to proliferating cholangiocytes and promote fibrosis.

75 tructural and functional phenotypes of large cholangiocytes and respond to secretin.

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

77 ary cirrhosis, four liver diseases affecting cholangiocytes and the biliary system.

78 nic stem cells (hESCs) to differentiate into cholangiocytes and we report a new approach, which drive

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

80 n of InsP3R3 in primary bile duct epithelia (cholangiocytes) and in the H69 cholangiocyte cell line,

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

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

83 o epithelial cell types such as hepatocytes, cholangiocytes, and oval cells.

84 nto other cell types, including hepatocytes, cholangiocytes, and progenitor cell types known as oval

85 r cells that give rise to adult hepatocytes, cholangiocytes, and SOX9(+) periductal cells.

86 Cholangiocytes are biliary epithelial cells, which, like

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

88 ecovering from DDC diet-induced injury, most cholangiocytes arose from Foxl1-Cre-marked HPCs.

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

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

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

92 e show that HDAC6 is overexpressed in cystic cholangiocytes both in vitro and in vivo, and its pharma

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

94 ly did IL-33 induce IL-6 expression by human cholangiocytes but it likely facilitated tumor developme

95 xendin-4-induced proliferation in normal rat cholangiocytes, but did not affect Ngn-3 synthesis.

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

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

98 gn-3 was knocked-down in vitro in normal rat cholangiocytes by short interfering RNA (siRNA).

99 te cell line, because the role of InsP3R3 in cholangiocyte Ca(2+) signaling and secretion is well est

100 hese data show that in fibrocystin-defective cholangiocytes, cAMP/PKA signaling stimulates pSer(675)

101 These findings demonstrate that mature cholangiocytes can be differentiated from hPSCs and used

102 more, experimentally induced senescent human cholangiocytes caused senescence in bystander cholangioc

103 In cholangiocytes, CCN1 activated NF-kappaB through integri

104 nRH receptors was assessed in a normal mouse cholangiocyte cell line (NMC), sham, and BDL rats.

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

106 ct epithelia (cholangiocytes) and in the H69 cholangiocyte cell line, because the role of InsP3R3 in

107 measuring calcium signaling in normal human cholangiocyte cells and secretion in isolated bile duct

108 oforms, but not miR-7b, was increased in DDC cholangiocytes compared to normal ones.

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

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

111 VCAM-1 expression by cholangiocytes contributes to persistent inflammation by

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

113 Subsequent to GABA in vitro treatment, small cholangiocytes de novo proliferate and acquire ultrastru

114 a concentration-dependent manner in multiple cholangiocyte-derived cell lines.

115 Interestingly, cultured cholangiocyte-derived cells did not accumulate appreciab

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

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

118 duodenal homeobox-1 (Hes-1/PDX-1) in mature cholangiocytes determines cell proliferation.

119 When grown in a 3D matrix, cholangiocytes developed epithelial/apicobasal polarity

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

121 Functional cholangiocyte differentiation was demonstrated via incre

122 EVs internalized by cholangiocytes drove cell proliferation and IL-6 secreti

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

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

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

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 In vivo, PSC cholangiocytes expressed significantly more senescence-a

130 disease, and chronic hepatitis C), and human cholangiocytes expressed VCAM-1 in response to tumor nec

131 Hence, in this study, we examined whether cholangiocyte expression of VCAM-1 promotes the survival

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

133 show that functionally impaired hPSC-derived cholangiocytes from cystic fibrosis patients are rescued

134 These conditions also allowed us to generate cholangiocytes from HepaRG-derived hepatoblasts.

135 s of Ngn-3 and miR-7 isoforms were tested in cholangiocytes from normal and cholestatic human livers.

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

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

138 differentiation of biliary epithelial cells (cholangiocytes) from human pluripotent stem cells (hPSCs

139 y biliary markers and mature CLCs displaying cholangiocyte functionality.

140 so displayed specific proteins important for cholangiocyte functions including cystic fibrosis transm

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

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

143 BDL cholangiocytes had increased expression of GnRH compared

144 We previously showed that cystic cholangiocytes have abnormal cell cycle profiles and mal

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

146 is, including that 1) the majority of distal cholangiocytes have stem-like properties, and 2) availab

147 d high levels of IL-13 that in turn promoted cholangiocyte hyperplasia.

148 d ACY-1215 decreased proliferation of cystic cholangiocytes in a dose- and time-dependent manner, and

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

150 We detected VCAM-1 on cholangiocytes in chronic liver disease (CLD) and hypoth

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

152 the role of melatonin synthesized locally by cholangiocytes in the autocrine regulation of biliary gr

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

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

155 Liver-derived T cells adhered to cholangiocytes in vitro by alpha4beta1, which resulted i

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

157 licate and differentiate into hepatocytes or cholangiocytes in vitro.

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

159 Cs, HSCs, and PFs, but not to hepatocytes or cholangiocytes, in the adult liver.

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

161 holangiocyte-like cells expressed markers of cholangiocytes including cytokeratin 7 and osteopontin,

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

163 CLCs show functional characteristics of cholangiocytes, including bile acids transfer, alkaline

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

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

166 We determined in coculture whether senescent cholangiocytes induce senescence in bystander cholangioc

167 in experimentally induced senescent cultured cholangiocytes; inhibition of Ras abrogated experimental

168 These results suggest that cholangiocyte injury may occur through lipoapoptosis in

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 established and because loss of InsP3R3 from cholangiocytes is responsible for the impairment in bile

176 xfold in cystic liver tissue and in cultured cholangiocytes isolated from both PCK rats (an animal mo

177 xtran sodium sulfate and in vitro in primary cholangiocytes isolated from wild-type and from Cftr-kno

178 omoter of ITPR3 to inhibit its expression in cholangiocytes, leading to reduced calcium signaling and

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

180 of human induced pluripotent stem cells into cholangiocyte-like cells (CLCs).

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

182 In addition, we showed that cholangiocyte-like cells could also be generated from hu

183 hESC- and HepaRG-derived cholangiocyte-like cells expressed markers of cholangioc

184 e consider that in addition to converting to cholangiocyte-like cells, Sox9(+)EpCAM(-) cells provide

185 differentiating pluripotent stem cells into cholangiocyte-like cells, which display structural and f

186 d/or hypertrophy but also by conversion into cholangiocyte-like cells.

187 giocytes, separates hepatocytic lineage from cholangiocyte lineage.

188 Here, we use a cholangiocyte-lineage tracing system to target p53 loss

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

190 capable of differentiating to hepatocyte and cholangiocyte lineages.

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

192 in NAFLD, we hypothesized the involvement of cholangiocyte lipoapoptosis as a mechanism of cellular i

193 aturated FFAs palmitate and stearate induced cholangiocyte lipoapoptosis by way of caspase activation

194 Palmitate and stearate induced cholangiocyte lipoapoptosis in a concentration-dependent

195 In addition, palmitate-induced cholangiocyte lipoapoptosis involved a time-dependent in

196 critical for palmitate- and stearate-induced cholangiocyte lipoapoptosis.

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

198 thelial structures expressing hepatocyte and cholangiocyte markers or resembling ectopic bile ducts d

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

200 The cholangiocyte membrane protein bound by SRL was found to

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

202 lrp3 knockdown increased the permeability of cholangiocyte monolayers.

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

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

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

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

207 he liver, Ngn-3 is expressed specifically in cholangiocytes of primary sclerosing cholangitis (PSC) p

208 ggestion that it is hepatocytes, rather than cholangiocytes or hepatic progenitor cells that represen

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

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

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

212 Hepatocytes, cholangiocytes, or macrophages are not the source of Wnt

213 iciently multipotent to produce hepatocytes, cholangiocytes, or oval cells by way of mesenchymal-epit

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

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

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

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

218 vation of the ERK/HIF-1alpha/VEGF pathway in cholangiocytes plays a key role during repair from bilia

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

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

221 We demonstrate that hPSC-derived cholangiocytes possess epithelial functions, including r

222 Cholangiocytes potentiated the angiogenic properties of

223 t, excessive commitment of hepatoblasts into cholangiocytes, premature intrahepatic bile duct morphog

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

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

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

227 , and its pharmacological inhibition reduces cholangiocyte proliferation and cyst growth.

228 These findings demonstrate that CCN1 induces cholangiocyte proliferation and ductular reaction and id

229 s and resolves liver fibrosis, also mediates cholangiocyte proliferation and ductular reaction, which

230 f GnRH decreased intrahepatic bile duct mass/cholangiocyte proliferation and fibrosis.

231 Cholangiocyte proliferation and interleukin 6 (IL-6) sec

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

233 ation of IL-33 to WT mice markedly increased cholangiocyte proliferation and promoted sustained cell

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

235 tion of CCN1 protein or soluble JAG1 induced cholangiocyte proliferation in mice, which was blocked b

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

237 Biliary mass and cholangiocyte proliferation were evaluated by immunohist

238 e peribiliary stem cell niche, regulation of cholangiocyte proliferation, and deposition of specific

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

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

241 autocrine role of GnRH in the regulation of cholangiocyte proliferation.

242 o Jag1 expression, JAG1/NOTCH signaling, and cholangiocyte proliferation.

243 ent activation of miR-7a is a determinant of cholangiocyte proliferation.

244 Here we investigated the role Ngn-3 on cholangiocyte proliferation.

245 hway and showed that RAGE activation induced cholangiocyte proliferation.

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

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

248 GnRH secreted by cholangiocytes promotes biliary proliferation via an aut

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

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

251 Cholangiocytes secrete proinflammatory cytokines during

252 Cholangiocytes secrete stem cell factor, which functions

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

254 ition of N-Ras with a resultant reduction in cholangiocyte senescence and SASP is a new therapeutic a

255 we explored signaling mechanisms involved in cholangiocyte senescence and SASP.

256 ) molecules normally present in bile induced cholangiocyte senescence and SASP.

257 We reported that cholangiocyte senescence features prominently in PSC and

258 Cholangiocyte senescence has been linked to primary scle

259 Cholangiocyte senescence induced by biliary constituents

260 Here we tested the hypothesis that cholangiocyte senescence is a pathophysiologically impor

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

262 Cholangiocyte senescence was significantly increased in

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

264 which blocked CDKN2A expression and reduced cholangiocyte senescence.

265 ssion of genes, which signed hESC- or HepaRG-cholangiocytes, separates hepatocytic lineage from chola

266 PC2-defective cholangiocytes show increased production of cyclic adeno

267 Large but not small cholangiocytes show inflammatory responses against large

268 In normal rat cholangiocytes, siRNA against Ngn-3 blocked the prolifer

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

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

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

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

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

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

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

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

277 opathies, a group of liver diseases in which cholangiocytes, the epithelia lining of the biliary tree

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

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

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

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

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

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

284 aintaining biphenotypic status can establish cholangiocyte-type polarity.

285 haracterized by progressive proliferation of cholangiocytes, ultimately causing hepatomegaly.

286 tors, hESCs were differentiated further into cholangiocytes using growth hormone, epidermal growth fa

287 on and secretion of GnRH in NMC and isolated cholangiocytes was assessed.

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

289 m and effects of parasite protein entry into cholangiocytes was unknown.

290 and subsequent lower melatonin secretion by cholangiocytes, was associated with increased biliary pr

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

292 Second, cholangiocytes were lineage traced with concurrent inhib

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

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

295 lls, capable of forming both hepatocytes and cholangiocytes when regeneration by mature hepatocytes i

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

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

298 Treatment of cholangiocytes with proinflammatory cytokines, nitric ox

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

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