ライフサイエンスコーパス: oval cell

1 tipotential nonparenchymal progenitor cells (oval cells).

2 ributing to differentiation of donor-derived oval cells.

3 on assays were performed on freshly isolated oval cells.

4 pes such as hepatocytes, cholangiocytes, and oval cells.

5 placement of hepatocytes, cholangiocytes, or oval cells.

6 s, but staining was substantially reduced in oval cells.

7 denced by a decreased number of OV6-positive oval cells.

8 xpression and localization of CTGF in Thy-1+ oval cells.

9 tocytes and thus appears to be selective for oval cells.

10 erential growth responses in hepatocytes and oval cells.

11 ted uniformly in all three subpopulations of oval cells.

12 tomy) had significantly increased numbers of oval cells.

13 solation of large numbers of highly purified oval cells.

14 number and maintained close association with oval cells.

15 aminin associated with single or clusters of oval cells.

16 n vivo and in vitro studies of mouse hepatic oval cells.

17 t time, very few markers exist for the mouse oval cells.

18 pha in the differentiation/maturation of rat oval cells.

19 es, biliary epithelial cells, and (ductular) oval cells.

20 liferation of cholangiocytes and intraportal oval cells.

21 cytoplasmic EpCAM(+)/HNF-4alpha(-) ductular oval cells.

22 initiated by the proliferation of so-called oval cells.

23 h is attributed to the specific expansion of oval cells.

24 resident stellate cells, myofibroblasts, and oval cells.

25 ogenitor cells, most likely endoderm-derived oval cells.

26 t migration but not proliferation on Thy1(+) oval cells.

27 , the PPARalpha activator induced, among the oval cells, a subpopulation of transitional cells showin

28 taminophen injury was followed by periportal oval cell accumulation displaying a moderate degree of m

29 Increased oval cell accumulation was accompanied by less hepatic n

30 During repair of the periportal zone, oval cells acquire differentiation markers of hepatocyte

31 CTGF and integrin alphavbeta6 regulate oval cell activation and fibrosis, probably through inte

32 Extensive oval cell activation and proliferation were observed at

33 ified a novel function of RAGE in regulating oval cell activation and tumor development in inflammati

34 or (CTGF), has been shown to be critical for oval cell activation during liver regeneration following

35 In conclusion, our studies indicate a marked oval cell activation during the height of hepatic injury

36 acologic blockade of RAGE signaling impaired oval cell activation in an independent mouse model of ov

37 ha-fetoprotein expression, implying impaired oval cell activation in these animals.

38 e ability to self-renew in all classic mouse oval cell activation injuries.

39 mediated liver regeneration does not require oval cell activation or proliferation.

40 pericentral hepatocytes during liver injury, oval cell activation, and hepatocyte regeneration.

41 Oval cell activation, as part of the regenerative proces

42 Hepatic expression of genes indicative of oval cell activation, as well as the number of cells exp

43 orted by NF-kappaB and STAT3 is required for oval cell activation, expansion, and differentiation.

44 ormal liver cells and at different stages of oval cell activation, indicating potential utility for p

45 activation in an independent mouse model of oval cell activation, the choline deficient ethionine-su

46 d integrin alphavbeta6 in hepatic progenitor/oval cell activation, which often occurs in the form of

47 thoxycarbonyl-1,4-dihydrocollidine to induce oval cell activation.

48 we assessed the involvement of G-CSF during oval cell activation.

49 up B received the 2-AAF/PHx required for the oval cell activation.

50 hat SDF-1 is an essential molecule needed in oval cell activation.

51 nchyma cells in prototypical mouse models of oval cell activation.

52 and fibrosis, in association with decreased oval cell activation.

53 adhesion and migration, thereby facilitating oval cell activation.

54 receptor system has been implicated in stem (oval) cell activation following liver injury in the rat.

55 During hepatic stem, or oval, cell activation, SDF-1 has been reported to be up-

56 rin alphavbeta6 could bind to CTGF mediating oval cell adhesion to CTGF and fibronection substrata an

57 ithin the liver, implying a possible role in oval cell-aided liver regeneration.

58 an FN-concentrated provisional matrix during oval cell-aided liver regeneration.

59 Ductular reactions are primarily composed of oval cells also known as "intermediate hepatobiliary cel

60 regeneration, and induces NK cell-sensitive oval cell and hematopoietic-like cell expansion followin

61 h reduced periductal accumulation of CD24(+) oval cells and abrogation of fibrosis.

62 rescent protein reporter mice suggested that oval cells and cholangiocytes were the main sources of C

63 ce staining for markers specific for hepatic oval cells and hepatocytes in serial sections, oval cell

64 ween TGF-beta signaling and proliferation in oval cells and hepatocytes, we examined TGF-beta signali

65 cterized epitope recognized by mouse hepatic oval cells and it is accepted to be an oval cell marker.

66 termediate or transitional cell type between oval cells and mature hepatocytes, rather than a distinc

67 bition would promote hepatic accumulation of oval cells and reduce liver damage in mice fed antioxida

68 through atypical ductular proliferation and oval cells and their subsequent differentiation to bile

69 ed hepatic accumulation of liver progenitor (oval) cells and oval cell numbers increased with the dem

70 typic characteristics of fetal hepatoblasts, oval cells, and fully differentiated hepatocytes, but di

71 firm colocalization of beta-catenin with the oval cell antigen A-6.

72 Oval cells appear and expand in the liver when hepatocyt

73 Hepatic progenitor/oval cells appear in injured livers when hepatocyte prol

74 Oval cells appear to be resistant to acetaminophen injur

75 ary injury, atypical ductular proliferation, oval cell appearance, and limited fibrosis.

76 We have shown that EpCAM(+) oval cells are bipotential adult hepatic epithelial prog

77 Oval cells are considered liver stem cells, a portion of

78 Adult hepatic stem cells or oval cells are facultative stem cells in the liver that

79 Oval cells are hepatocytic precursors that proliferate i

80 roliferation, and differentiation of hepatic oval cells are not fully understood.

81 Oval cells are postnatal hepatic progenitors with high p

82 Oval cells are resident hepatic stem cells that promote

83 These results show that oval cells are responsive to PPs and strongly argue for

84 Also, there were smaller oval cell areas, fewer proliferating ductular epithelial

85 ls are elevated in chronic liver injury when oval cells arise, we hypothesized that oval cells may be

86 and compensatory hyperplasia of progenitor (oval) cells as a reaction to chronic injury due to ongoi

87 The oval cells at the proximal tips of the ductules have a m

88 cells expressing Sca-1/CD34/CD45 were indeed oval cells because they co-expressed the oval cell-speci

89 that the cells expressing Thy-1 were indeed oval cells, because they also expressed alpha-fetoprotei

90 onstrated a critical role of beta-catenin in oval cell biology.

91 deutocerebral commissure consisted of small oval cell bodies and strands that formed a reticulated p

92 keratin 19-positive bile ductule-like cells (oval cells) both in portal regions and extending into th

93 Our results indicate that oval cells, both in vivo and in vitro, are less sensitiv

94 These findings highly suggest the hepatic oval cells but not mature hepatocytes as the origin of S

95 g evidence that SHPCs are not the progeny of oval cells but represent a distinct population of liver

96 t to produce hepatocytes, cholangiocytes, or oval cells by way of mesenchymal-epithelial transition i

97 Oval cells can potentially become either hepatocytes or

98 hepatocyte hypertrophy; 2) activation of the oval cell compartment and subsequent maturation to hepat

99 t model has been established to activate the oval cell compartment in mice by incorporating 3,5-dieth

100 liver triggers activation of the progenitor (oval) cell compartment and a severe fibrogenic response.

101 Oval cells constitute a reserve compartment that is acti

102 ation of all cell types peaks at 2 days, but oval cells continue to proliferate and differentiate thr

103 ly, TWEAK stimulated the proliferation of an oval cell culture model.

104 ved at this time, which was localized to the oval cell cytoplasm and nuclei by immunohistochemistry a

105 In a pilot study, the oval cell-derived islet cell-like clusters displayed the

106 ration of bile epithelial-like cells (termed oval cells), development of foci composed of small hepat

107 aled that they represent different stages of oval cell differentiation along hepatocyte lineage.

108 novel findings implicating Wnt1 in directing oval cell differentiation during the rat 2-acetylaminofl

109 Oval cells do not express previously reported hematopoie

110 We conclude that hepatic oval cells do not originate in bone marrow but in the li

111 verely impaired and massive proliferation of oval cells does not occur.

112 production of hepatocytes, biliary cells, or oval cells during liver regeneration.

113 r the efficient regeneration of the liver by oval cells during massive hepatic injury.

114 Oval cell expansion induced by 3,5-diethoxycarbonyl-1,4-

115 Progenitor ("oval") cell expansion accompanies many forms of liver in

116 However, oval cells express a number of mesenchymal markers inclu

117 We report herein that mouse oval cells express high levels of Sca-1 and CD34, as wel

118 Sorted Thy-1+ oval cells expressed a high level of CTGF gene in a quan

119 Oval cells expressed high RAGE levels and displayed redu

120 Oval cells expressed low levels of albumin and thereby e

121 In the absence of Wnt1 signaling, oval cells failed to differentiate into hepatocytes and

122 xpressed at relatively low levels in primary oval cells from rats fed the CDE diet alone.

123 A group of novel differentially expressed oval cell genes is also presented.

124 Tgfa, and Tweak) for proteins that maintain oval cell growth and differentiation.

125 patocytes and intrahepatic progenitor cells (oval cells) have similar responses to most growth factor

126 Proliferating ducts, termed "oval cells," have long been thought to be bipotential, t

127 ells migrate into the liver and give rise to oval cells, hepatocytes, and biliary epithelial cells.

128 Hepatic oval cells (HOC) are a small subpopulation of cells foun

129 Hepatic oval cells (HOC) are thought to be a type of facultative

130 SNS signaling affects hepatic progenitor/oval cells (HPCs) and beta-adrenoceptor agonism will exp

131 Liver lesions consisted of Kupffer, Ito, and oval cell hyperplasia along with multifocal to coalescin

132 s, lymphocytic inflammation, focal necrosis, oval cell hyperplasia, and fibrosis.

133 sing TWEAK in hepatocytes exhibit periportal oval cell hyperplasia.

134 had histological evidence of karyomegaly and oval cell hyperplasia.

135 K-19), OC.2, and OV-6, all known markers for oval cell identification.

136 nderlying mechanism for the proliferation of oval cells in an environment inhibitory to hepatocytic p

137 The appearance of bipotential oval cells in chronic liver injury suggests the existenc

138 Increased proliferation of oval cells in IL-6 knockout mice may compensate for the

139 neration of hepatocytes, cholangiocytes, and oval cells in immune-deficient adult animals after neona

140 vous system inhibition reduces the number of oval cells in injured livers.

141 liferation were compensated by a response of oval cells in Nemo(Deltahepa) mice.

142 ation of adult facultative stem cells termed oval cells in periductal regions.

143 a expression was augmented in bile ducts and oval cells in retrorsine/partial hepatectomy-treated liv

144 e recently, recognition of the role of small oval cells in the carcinogenic process led to a new hypo

145 previous reports, suggest the involvement of oval cells in the hepatocarcinogenicity of PPs.

146 feration of hepatocytes, cholangiocytes, and oval cells in the livers of normal control to those of i

147 tor decreased the sphere-forming capacity of oval cells in vitro as well as reduced oval cell pool, i

148 acted as a chemoattractant and a mitogen for oval cells in vitro.

149 ate genes differentially expressed in Thy-1+ oval cells, in this liver injury model.

150 First, the oval cells increased in number and often formed ductules

151 physiological requirement of Wnt1 during the oval cell induction.

152 Because oval cells induction is commonly associated with liver i

153 uency of one of 34 or one of 25 in normal or oval cell injury livers, respectively.

154 Sox9(+) cells were traced in multiple oval cell injury models using both histology and fluores

155 <1%) to the hepatocyte pool, even in classic oval cell injury models.

156 e of hepatocyte-driven regeneration in mouse oval cell injury models.

157 he bone marrow cells are a source of hepatic oval cells involved in rat liver regeneration induced by

158 Recruitment and proliferation of Thy-1+ oval cells is a hallmark of liver regeneration after 2-a

159 The precursor to oval cells is considered to be a facultative liver stem

160 normal mice, whereas the number of dividing oval cells is higher.

161 Oval cells isolated from DDC-fed mouse livers showed the

162 d the PPARalpha-mediated response of primary oval cells isolated from rats fed a choline-deficient et

163 for CD34 and CD45, we have developed a rapid oval cell isolation protocol with high yields of greater

164 ized lines of hepatocytes (AML-12 cells) and oval cells (LE-6 cells) to investigate the potential mec

165 etreatment increased the numbers of separate oval cell-like CD117(+) cells and hematopoietic-like Sca

166 of diseased uPA-expressing liver induces an oval cell-like response, as observed in other models of

167 rogenitors within 1 week through a transient oval cell-like stage.

168 The LE/2 and LE/6 oval cell lines used in this study are nontumorigenic ce

169 Two oval cell lines, LE/2 and LE/6, were less responsive.

170 c differentiation from precursor epithelial (oval) cell lines.

171 in vivo exposure to Wnt1 shRNA inhibited rat oval cell liver regeneration.

172 In this study, the rat oval cell marker, OV-6 has been used to investigate the

173 s the number of cells expressing A6, a mouse oval cell marker, was greater in egr-1(-/-) mice.

174 patic oval cells and it is accepted to be an oval cell marker.

175 EpCAM(+) cells express the classical oval cell markers (alpha-fetoprotein, cytokeratin-19, OV

176 markers (including hepatocyte and bile duct-oval cell markers), and established in short-term primar

177 and by low expression of hepatocyte markers, oval cell markers, and stellate cell markers.

178 when oval cells arise, we hypothesized that oval cells may be less responsive to the growth inhibito

179 and activator of transcription 3 (STAT3) in oval cell-mediated liver regeneration induced by 2-acety

180 ylaminofluorene/partial hepatectomy model of oval cell-mediated liver regeneration, followed by admin

181 Progenitor (oval) cell mitogen tumor necrosis factor-like weak induc

182 nt two different populations of cells in the oval cell niche.

183 Thus, neither oval cell nor BEC proliferation, nor hepatocyte hypertro

184 mpathetic nervous system (SNS) inhibition on oval cell number is not known.

185 essage increased coinciding with the rise in oval cell number, whereas protein levels peaked immediat

186 A dramatic decrease in the A6-positive oval cell numbers in the absence of beta-catenin demonst

187 ulation of liver progenitor (oval) cells and oval cell numbers increased with the demand for hepatocy

188 Hepatic progenitor/oval cell (OC) activation occurs when hepatocyte prolife

189 3b, is crucial in the ductular reaction (DR)/oval cell (OC) response for generating new hepatocyte li

190 essing cells proliferate in the liver during oval cell (OC)-mediated liver regeneration.

191 enitor cells, is also expressed in activated oval cells of rat liver.

192 ilize facultative stem cells, also known as "oval cells" or "atypical ductal cells" (ADCs), for regen

193 To determine whether oval cells originated from stem cells residing in the bo

194 cytokeratins, as both number and density of oval cells per portal tract, analyzed by size of portal

195 ty of oval cells in vitro as well as reduced oval cell pool, impaired migration, and decreased hepato

196 Group B showed that approximately 20% of the oval cell population expressed both donor marker (DPPIV)

197 pecific for regenerating livers with massive oval cell presence.

198 le, and triple staining to study lineages of oval cells present in DRs.

199 intrahepatic biliary tree, identification of oval cells (presumed progeny of hepatic stem cells) in a

200 se and generated NO, while similarly treated oval cells produced little if any NO.

201 t models of hepatocarcinogenesis and injury, oval cells proliferate in the periportal regions of the

202 through replication of existing hepatocytes, oval cells proliferate only when hepatocyte proliferatio

203 as associated with a significant decrease in oval cell proliferation and a lower level of alpha-fetop

204 ductal progenitor cells give rise to clonal oval cell proliferation and bipotential organoids, but r

205 of age demonstrated a robust and widespread oval cell proliferation followed by cholangiofibrosis an

206 l cycle arrest in hepatocytes but stimulates oval cell proliferation in cultured cells.

207 F-like weak inducer of apoptosis) stimulates oval cell proliferation in mouse liver through its recep

208 a regimen commonly used for the induction of oval cell proliferation in rodents) with or without cotr

209 There was no evidence of oval cell proliferation in the IL-6(-/-) mice, as determ

210 HMGB1 promoted an ERK1/2-Cyclin D1-dependent oval cell proliferation in vitro.

211 The regulation of oval cell proliferation is incompletely understood.

212 sibility through the targeted elimination of oval cell proliferation secondary to bile duct destructi

213 igin and properties of this cell population, oval cell proliferation was induced in adult mouse liver

214 remained virtually unaffected, with minimal oval cell proliferation, only occasional and small foci

215 ic injury, including inflammation, necrosis, oval cell proliferation, or scarring.

216 feration, and then hepatic injury, to induce oval cell proliferation.

217 hepatocyte proliferation and stimulation of oval cell proliferation.

218 evels peaked immediately after the height of oval cell proliferation.

219 ne (DDC)-enriched diet was used to stimulate oval cell proliferation.

220 al cells and hepatocytes in serial sections, oval cell proliferations with CK-19(+)/laminin(+) and OV

221 The timing of the two peaks of the oval cell reaction also changed with increasing dose, th

222 The oval cell reaction was quantified, on immunostaining for

223 ficantly increased both the magnitude of the oval cell reaction, and the contribution of BM to liver

224 The magnitude of oval cell reaction, the entity of BM contribution to liv

225 e liver, as well as enhancing the endogenous oval cell reaction.

226 n through the generation of NO and stimulate oval cell replication.

227 It has been proposed that these oval cells represent transitional cells in a nonhepatocy

228 The adhesion of these two modules on Thy1(+) oval cells required heparan sulfate proteoglycan and int

229 From these data, we conclude that oval cells respond to Wnt ligands (Wnt3a) in vitro with

230 that CTGF induction is important for robust oval cell response after 2-AAF/PHx treatment in rats.

231 trilobular damage results in a more enhanced oval cell response and AFP gene expression than periport

232 The oval cell response and AFP gene expression was ranked as

233 r objective in this study was to examine the oval cell response and associated alpha-fetoprotein (AFP

234 The age dependence of the oval cell response and bile duct carcinomas of male F344

235 ed beginning at 8 weeks of age had much less oval cell response and cholangiofibrosis with only 1 of

236 osed to cyclic CDE diet display a diminished oval cell response and fewer CCAs.

237 rom normal adult mice or those undergoing an oval cell response and tested their capacity to form bil

238 Extensive elimination of oval cell response by repeated administration of 4,4'-me

239 odies to support investigation of the murine oval cell response has been developed.

240 Moreover, the oval cell response to WY14,643 was accompanied by an ove

241 Oval cell response was biphasic, not temporally correlat

242 The oval cell response was compromised in these animals, as

243 as accompanied by a robust activation of the oval cell response, suggesting more severe liver injury

244 To see a true oval cell response, the hepatocytes must be inhibited fr

245 face reactive reagents more specific for the oval cell response, we generated a new collection of mon

246 the role of the Wnt/beta-catenin pathway in oval cell response, which was initiated in male Fisher r

247 ats to investigate the effect of Iloprost on oval cell response.

248 the damaged rat liver by contributing to the oval cell response.

249 both CCl(4)-induced hepatic fibrosis and the oval cell response.

250 mma) increases in liver injury that involves oval cell responses, but it is not upregulated during li

251 tential lineage relationship between hepatic oval cells, small hepatocyte-like progenitor cells (SHPC

252 eed oval cells because they co-expressed the oval cell-specific marker A6 (94.57% +/- 0.033%), as wel

253 to thymus cell antigen 1-positive (Thy1(+)) oval cells, stellate cells, and sinusoidal endothelial c

254 arked induction of the peripheral periductal oval cell/stem cell compartment of the liver.

255 ysis of these cells showed that they express oval cell/stem cell markers such as CD90 (Thy-1), CD34,

256 her types of HCC included markers of hepatic oval cells, suggesting that HCC of this subtype may aris

257 In this work, we studied progenitor/oval cell surface markers in the liver of rats subjected

258 The specificity of progenitor/oval cell surface markers was confirmed by ISH and doubl

259 ring filament maturation result in round and oval cells surrounding and covering the pseudohyphal fil

260 iation of hepatic stem cell progenies (i.e., oval cells) sustain liver regeneration when the replicat

261 n contrast, was significantly more common in oval cells than hepatocytes.

262 knockout (KO) mice led to fewer A6-positive oval cells than wildtype (WT) littermates.

263 K has a selective mitogenic effect for liver oval cells that distinguishes it from other previously d

264 Repopulation of the liver with oval cells that expressed NEMO reversed liver damage in

265 We examined the response of murine oval cells, that is, the putative liver progenitor cells

266 with WY14,643 for 2-6 weeks induced, in the oval cells, the expression of PPARalpha as well as that

267 To activate oval cells, the hepatic stem cell (HSC) progeny, we used

268 giocytes, and progenitor cell types known as oval cells, thereby acting as stem cells in the liver.

269 nuclear translocation of beta-catenin within oval cells throughout the 2AAF/PHx protocol.

270 The response of hepatocytes and oval cells to cytokine combinations may contribute to th

271 y, inhibition of Wnt1 resulted in failure of oval cells to differentiate into hepatocytes and alterna

272 The terms oval cell, transitional hepatocyte, biliary hepatocyte,

273 ion, we studied the role of Wnt signaling in oval cells using a mouse model of chronic liver injury.

274 Deletion of c-met in oval cells was confirmed in both models by polymerase ch

275 ion of the mesodermal mesenchymal cells into oval cells was not observed.

276 g with increased expression of Frizzled-2 in oval cells was observed.

277 To examine TGF-beta signaling in vivo in oval cells, we analyzed livers of rats fed a choline-def

278 s a marker for identification and sorting of oval cells, we established that both NF-kappaB and STAT3

279 hybridization further confirmed that Thy-1+ oval cells were a source of CTGF.

280 Oval cells were activated in 2-acetylaminofluorene-treat

281 ompetitive repopulation experiments, hepatic oval cells were at least as efficient as mature hepatocy

282 Three distinct subpopulations of oval cells were defined as OV1(low), OV1(medium), and OV

283 rare clones containing both hepatocytes and oval cells were found in any experiment.

284 Oval cells were found to express G-CSF receptor and G-CS

285 Increases in oval cells were largely confined to the smallest portal

286 Oval cells were never seen in the livers of DAPM-treated

287 In mice with chimeric livers, the oval cells were not derived from hepatocytes but from li

288 n appearance or numbers of total A6-positive oval cells were observed after DDC administration.

289 mice were treated with DDC for 8 months and oval cells were then serially transferred into Fah mutan

290 feration indices, including proliferation of oval cells, were markedly increased and correlated with

291 ls, which share phenotypic similarities with oval cells, were previously reported to be capable of fo

292 was to investigate the role of PPARalpha in oval cells, which are considered to be closely related t

293 mical and ultrastructural characteristics of oval cells, which are multipotent cells that can differe

294 face markers specific for hepatic progenitor/oval cells, which offers powerful tool for their identif

295 ic to the basket cells: large (20-30-microm) oval cells with dark cytoplasm, and large oval cells wit

296 Moreover, stimulation of oval cells with HMGB1 promoted an ERK1/2-Cyclin D1-depen

297 ysaccharide content, more round cells versus oval cells with OG1RF, decreased biofilm formation, atte

298 m) oval cells with dark cytoplasm, and large oval cells with paler cytoplasm, often with an apical de

299 ls in group C failed to significantly induce oval cells with the donor DPPIV antigen.

300 catenin signal transduction in proliferating oval cells within atypical ductal proliferations (ADPs).