ライフサイエンスコーパス: HSC

1 HSC play a crucial role in the cellular crosstalk of rap

2 HSCs from Fgf15(-/-) mice showed increased FXR activity

3 HSCs interact with BM niche cells that produce growth fa

4 HSCs keep and accumulate dysfunctional mitochondria thro

5 HSCs present a complex variety of regenerative behaviour

6 HSCs treated with the key RET ligand/coreceptor complex,

7 HSCs were isolated 24 hours later, and fibrogenic/inflam

8 one sections from different bone types and 3 HSC reporter lines.

9 ceptor CXCR4 and integrins rapidly abrogated HSC motility and shape dynamics in real time.

10 d increases the number of cells that acquire HSC activity.

11 Activated HSCs show limited response to OCA and other FXR agonists

12 Up-regulation of PFKFB3 in activated HSCs did not occur via increased transcription, but inst

13 chanisms and the function of Prdm16 in adult HSCs remain unclear.

14 optosis between wild-type and knockout adult HSCs.

15 oiesis and lack of beta4GalT1 further affect HSC homeostasis.

16 ereby increasing the efficacy of OCA against HSC activation and fibrosis.

17 poiesis is not an intrinsic property of aged HSCs, but associated with decreased levels and functiona

18 e revealed transcriptional differences among HSCs, providing a possible explanation for their functio

19 te to control cytoplasmic Cdc42 activity and HSC fate determination in vivo.

20 mmation adversely impacts niche activity and HSC function which is reversible upon suppression of inf

21 e and the data from fate tracking of EMP and HSC lineages indicated the possibility of cell-cell fusi

22 crosstalk between hepatocyte metabolism and HSC senescence that promotes tumour growth.

23 ads to complete loss of HSC self-renewal and HSC depletion.

24 ubstantially faster than at steady-state and HSC function is drastically affected.

25 O-A/TPH1 are expressed in cholangiocytes and HSCs from BDL rats and Mdr2(-/-) (-) mice.

26 gnalling leads to reversal of age-associated HSC platelet lineage bias, increased generation of lymph

27 ot well understood, and therapies to augment HSC DNA repair following myelosuppression remain undevel

28 C) vascular niche regulating balance between HSC self-renewal and commitment.

29 3 enhanced the expansion of human cord blood HSCs without losing cell viability in vitro.

30 In contrast, cycling juvenile BM HSCs preferentially located close to Cxcl12 stroma and f

31 by the increased expression of Collagen-I by HSCs incubated with either a phosphorylated or nonphosph

32 c acid (OCA) prevents hepatic stellate cell (HSC) activation and fibrogenesis.

33 tigated mechanisms of hepatic stellate cell (HSC) activation, which contributes to liver fibrogenesis

34 hepatocyte-macrophage-hepatic stellate cell (HSC) crosstalk.

35 Hematopoietic stem cell (HSC) attrition is considered the key event underlying pr

36 myeloid bias of the hematopoietic stem cell (HSC) compartment, causing increased risk of immune compr

37 reactions and cause hematopoietic stem cell (HSC) exhaustion; therefore, IFN-I expression must be tig

38 ave identified that hematopoietic stem cell (HSC) fitness response to stress depends on Yap1 and Taz.

39 tical regulators of hematopoietic stem cell (HSC) function during diverse processes including embryon

40 lammation, impaired hematopoietic stem cell (HSC) function, and increased incidence of myeloid malign

41 dependently of the haematopoietic stem cell (HSC) lineage and the data from fate tracking of EMP and

42 constituent of the hematopoietic stem cell (HSC) niche.

43 and regulating the hematopoietic stem cell (HSC) niche.

44 erty that maintains hematopoietic stem cell (HSC) potency throughout life.

45 of the bone marrow hematopoietic stem cell (HSC) vascular niche regulating balance between HSC self-

46 that controls the haematopoietic stem cell (HSC)-niche interaction and determines the fate of HSCs.

47 +)CD41(+)CD16/32(+) hematopoietic-stem-cell (HSC)-independent erythro-myeloid progenitors (EMPs) pres

48 Hepatic stellate cells (HSC) are the major cellular contributors to excess extra

49 Hematopoietic stem cells (HSC) self-renew to sustain stem cell pools and different

50 FXR activation in hepatic stellate cells (HSCs) reduces liver fibrosis (LF).

51 on and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-associated secretory phen

52 n cultured activated hepatic stellate cells (HSCs), we show that OPN, besides being overexpressed, is

53 f cholangiocytes and hepatic stellate cells (HSCs).

54 enetic labeling of hematopoietic stem cells (HSCs) and distinguishes HSC-derived monocytes from micro

55 Hematopoietic stem cells (HSCs) are regulated by signals from the bone marrow (BM)

56 hat accumulate in haematopoietic stem cells (HSCs) are thought to be responsible for age-related chan

57 How transplanted haematopoietic stem cells (HSCs) behave soon after they reside in a preconditioned

58 onditions in which hematopoietic stem cells (HSCs) can be expanded for clinical benefit are highly so

59 wing capabilities, hematopoietic stem cells (HSCs) can maintain hematopoiesis throughout life.

60 ic requirements of hematopoietic stem cells (HSCs) change with their cell cycle activity.

61 Hematopoietic stem cells (HSCs) develop from the hemogenic endothelium in cluster

62 The biology of haematopoietic stem cells (HSCs) has predominantly been studied under transplantati

63 Fetal and adult hematopoietic stem cells (HSCs) have distinct proliferation rates, lineage biases,

64 emains unclear how hematopoietic stem cells (HSCs) in the bone marrow (BM) sense peripheral inflammat

65 ct localization of hematopoietic stem cells (HSCs) in their native bone marrow (BM) microenvironment

66 ed gene editing in hematopoietic stem cells (HSCs) is a promising treatment for several diseases.

67 Expansion of human hematopoietic stem cells (HSCs) is a rapidly advancing field showing great promise

68 ment downstream of hematopoietic stem cells (HSCs) is commonly hijacked in myeloid malignancies.

69 mutations arise in hematopoietic stem cells (HSCs) many years before malignancies develop, but diffic

70 7Ra) expression on hematopoietic stem cells (HSCs) mediates changes in HSCs that occur in old age, in

71 As humans age, hematopoietic stem cells (HSCs) occasionally acquire mutations in genes including

72 Hematopoietic stem cells (HSCs) remain quiescent to preserve long-term integrity.

73 Haematopoietic stem cells (HSCs) reside in specialized microenvironments in the bon

74 Hematopoietic stem cells (HSCs) reside in the bone marrow (BM) stem cell niche, wh

75 ty of multipotent haematopoietic stem cells (HSCs) supports blood system homeostasis throughout life

76 is is governed by haematopoietic stem cells (HSCs) that produce all lineages of blood and immune cell

77 ctions of residual hematopoietic stem cells (HSCs) within the leukemic niche are poorly understood, e

78 ause DNA damage to hematopoietic stem cells (HSCs), leading to HSC depletion and dysfunction and the

79 iver mutations in haematopoietic stem cells (HSCs).

80 intenance of adult hematopoietic stem cells (HSCs).

81 vels and perturbed hematopoietic stem cells (HSCs).

82 uman (CD34(+), CD133(+), and ALDH(hi) cells) HSC self-renewal ex vivo.

83 ffer cells), LECs (Liver Endothelial Cells), HSCs (Hepatic Stellate Cells) and/or myofibroblasts to m

84 Distinctive from other tissue stem cells, HSCs transition through multiple hematopoietic sites dur

85 as measured with the Highly Sensitive Child (HSC) questionnaire and heritability estimates were obtai

86 underlies the curative capacity of clinical HSC transplantation therapies.

87 orate T cells into human 3D skin constructs (HSCs), which enabled us to closely monitor and quantitat

88 he functional pool of th3 HSCs by correcting HSC-niche cross talk.

89 otch and Wnt signaling that prevent damaging HSC function, MPP production, and blood output in condit

90 ther transcriptomic study revealed decreased HSC signatures in long-term HSCs from the Hopx(-/-) mice

91 molecule inflachromene limits FBP1-dependent HSC activation, the subsequent development of the senesc

92 using increased HSC DNA damage and depressed HSC recovery over time.

93 ight how mitochondrial metabolism determines HSC fate, and especially focus on the links between mito

94 opoietic stem cells (HSCs) and distinguishes HSC-derived monocytes from microglia and other tissue-re

95 identity, and allowed highly efficient donor-HSC engraftment without irradiation.

96 TCF15 to be required and sufficient to drive HSC quiescence and long-term self-renewal.

97 one type of HSC divisional memory and drives HSC attrition.

98 out of Sel1L in hematopoietic tissues drives HSCs to hyperproliferation, which leads to complete loss

99 Much less is known about mechanisms driving HSC development in humans.

100 lysis were early and sustained events during HSC activation and accompanied by increased expression o

101 en particularly challenging to study dynamic HSC behaviour, given that the visualization of HSCs in t

102 The large numbers of expanded HSCs enable HSC transplantation into nonconditioned recipients, whic

103 otherapy alone, whilst protecting endogenous HSC.

104 f nociceptive neurons-significantly enhanced HSC mobilization in mice.

105 den upon LCMV infection but show exacerbated HSC activation under systemic poly(I:C)-induced inflamma

106 The large numbers of expanded HSCs enable HSC transplantation into nonconditioned reci

107 -resorbing activity do not harbour expanding HSCs.

108 d production of IL6 in gingival fibroblasts, HSC-2 and RAW 264.7 cells.

109 feasible alternative to nuclease editing for HSC-targeted therapeutic genome modification.

110 nal efficiencies (TEs) of mRNAs required for HSC maintenance.

111 ansiently triggers myeloid regeneration from HSCs in response to stress, and that constitutive low No

112 SABER reproducibly quantifies functional HSCs and can accommodate a wide range of experimental gr

113 gle-cell transcriptome of in vitro-generated HSC-like cells with those generated within the fetal liv

114 ishable localization from alpha-catulin-GFP+ HSCs.

115 transcriptional classifications, most homed HSCs in bone marrow and spleen became multipotent progen

116 (2020), we can all now see how HSCs behave in their niches!

117 derwent changes that were conserved in human HSC.

118 as an important secreted regulator of human HSC development.

119 Furthermore, we compared profiling of human HSC microRNAs with that of rat HSC so as to identify tho

120 o identify secreted signals underlying human HSC development, we combined spatial transcriptomics ana

121 ell lines of murine cholangiocytes and human HSCs express 5HTR2A/2B/2C and MAO-A/TPH1; treatment of t

122 r, EGF treatment drove the recovery of human HSCs capable of multilineage in vivo repopulation follow

123 ential agents for ex vivo expansion of human HSCs.

124 -2 cells and culture-activated primary human HSCs.

125 ultilineage-repopulating self-renewing human HSCs with high frequency as assayed in primary and secon

126 oposed as a driver of age-related changes in HSC function and myeloid malignancy, but mechanisms link

127 endoplasmic reticulum (ER), and lysosomes in HSC metabolism.

128 tive to DNMT3A loss after DNMT3A ablation in HSCs and in leukemia samples.

129 Repression of lysosomal activation in HSCs led to further enlargement of lysosomes while suppr

130 of label induction, accumulated with age in HSCs with high repopulation potential.

131 support a profibrotic role of PDGFR-alpha in HSCs during chronic liver injury in vivo via regulation

132 To examine the role of PDGFR-alpha in HSCs, Lrat-Cre recombinase and Pdgfra-floxed mice were b

133 arate functions in LSCs as they often are in HSCs.

134 oietic stem cells (HSCs) mediates changes in HSCs that occur in old age, including myeloid skewing, r

135 regeneration and early lineage decisions in HSCs and could be targeted in LSCs to normalize leukemic

136 Our findings reveal a defect in HSCs in beta-thalassemia induced by an altered BM microe

137 ed branch of ERAD(4), is highly expressed in HSCs.

138 r types of liver injury, PDGFR-alpha loss in HSCs led to a significant albeit transient reduction in

139 ctor receptor (EGFR) regulates DNA repair in HSCs following irradiation via activation of the DNA-dep

140 RASPs negatively regulate CXCR4 stability in HSCs.

141 s are enriched in the quiescent and inactive HSCs, and conditional knockout of Sel1L in hematopoietic

142 lection for specific mutations that increase HSC competitive fitness, in conjunction with additional

143 linked to decreased quiescence and increased HSC activity in bone marrow transplantation.

144 ity following irradiation, causing increased HSC DNA damage and depressed HSC recovery over time.

145 rachloride injury, associated with increased HSC death and reduced migration.

146 te colony-stimulating factor (G-CSF)-induced HSC mobilization via the secretion of calcitonin gene-re

147 A GalR2 antagonist inhibited HSC activation when Gal was administered directly to LX-

148 1 and Rab5a represent targets for inhibiting HSC activation and the hepatic tumor microenvironment.

149 powerful approach with which to interrogate HSC self-renewal and lineage commitment and, more broadl

150 ammation and fibrogenesis; and insights into HSC and macrophage heterogeneity revealed by single-cell

151 microscopy to visualize genetically labeled HSCs in the BM of live mice for several hours.

152 livers and reconstructed the single-lineage HSC trajectory from pericyte to myofibroblast.

153 topoietic stem cells (pre-HSCs), fetal liver HSCs, and adult bone marrow HSCs.

154 shown to cause a severe loss of fetal liver HSCs; however, the underlying mechanisms and the functio

155 LT-HSCs are not found in bone marrow niches with the deepes

156 Activated LT-HSCs show heterogeneous responses, with some cells becom

157 set of the most quiescent long-term HSCs (LT-HSCs) and that is compatible with current intravital ima

158 We show that this subset of LT-HSCs resides close to both sinusoidal blood vessels and

159 In vivo time-lapse imaging revealed that LT-HSCs at steady-state show limited motility.

160 d studies with primary mouse HSCs, human LX2 HSCs, human cirrhotic liver tissues, rats and mice with

161 Knockdown of CPEB4 in LX2 HSCs prevented PFKFB3 overexpression and cell activation

162 HSC regenerative potential while maintaining HSC quiescence.

163 Cs), fetal liver HSCs, and adult bone marrow HSCs.

164 elop inhibitors of MEIS1 that could modulate HSC activity.

165 Molecularly, HSCs carrying dysfunctional mitochondria can re-enter qu

166 Ps) have been demonstrated to regulate mouse HSC self-renewal and stemness, we screened small molecul

167 try of mouse young adult and old adult mouse HSCs, multipotent progenitors and oligopotent progenitor

168 nscriptional repression in young adult mouse HSCs.

169 atform for the expansion of functional mouse HSCs ex vivo for >1 month under fully defined albumin-fr

170 rt proteomic coverage of young and old mouse HSCs and progenitors, with broader implications for unde

171 We performed studies with primary mouse HSCs, human LX2 HSCs, human cirrhotic liver tissues, rat

172 he most primitive subset of true multipotent HSCs.

173 s for tracking the mitotic history of murine HSCs in label dilution experiments.

174 Here we show that murine HSCs and committed hematopoietic progenitor cells (HPCs)

175 the regulatory programs that guide neonatal HSC/HPC ontogeny, but it creates heterogeneity within th

176 underscore the importance of accessory, non-HSC to accelerate hematopoietic engraftment.

177 ways in which LSCs take advantage of normal HSC properties to promote survival and expansion, thus u

178 key regulator of bone metabolism but also of HSC activity.

179 h and is also amenable to clonal analysis of HSC heterogeneity.

180 s myelopoiesis and transcriptome analysis of HSC/GMP cell populations revealed enrichment of neutroph

181 Using single-cell assays of HSC quiescence, stemness, differentiation potential, and

182 splay altered expression as a consequence of HSC transdifferentiation and of these 104 were modulated

183 fies widespread changes in the expression of HSC microRNAs in fibrogenesis, but suggests a need for c

184 displacement of HSCs and a complete loss of HSC identity, and allowed highly efficient donor-HSC eng

185 ate that inactivation of Drp1 causes loss of HSC regenerative potential while maintaining HSC quiesce

186 oliferation, which leads to complete loss of HSC self-renewal and HSC depletion.

187 and embryonic fetal liver, the mechanism of HSC self-renewal has remained elusive.

188 udies aiming to understand the mechanisms of HSC clonal evolution will benefit from this new approach

189 rmaceuticals to be utilized in modulation of HSC activity and bone marrow transplantation studies.

190 e use gene mapping to identify modulators of HSC biology linked to MPN risk, and show through targete

191 Extrinsic regulation of HSC DNA repair is not well understood, and therapies to

192 ronic liver injury in vivo via regulation of HSC survival and migration and affect the immune microen

193 degradation of CXCR4, a master regulator of HSC function during transplantation.

194 dies identified MPL, the master regulator of HSC identity(5), as a bona fide ERAD substrate that beca

195 cell niche, which provides a vital source of HSC regulatory signals.

196 lls representing key developmental stages of HSC ontogeny in mice.

197 al morphology and segregation is one type of HSC divisional memory and drives HSC attrition.

198 Review presents our current understanding of HSC self-renewal in vivo and ex vivo, and discusses impo

199 mDia1) for the myofibroblastic activation of HSCs.

200 th implications for clinical applications of HSCs and other stem cells.

201 de population and reconstitution capacity of HSCs were significantly decreased in Tet1(-/-) mice.

202 letion of Sel1l led to niche displacement of HSCs and a complete loss of HSC identity, and allowed hi

203 Our data do not support abrupt entry of HSCs into permanent quiescence or sudden loss of regener

204 of HSCs and the modest ex vivo expansion of HSCs in media that contain poorly defined albumin supple

205 mRNA expression of HSCs activation markers and FXR engagement were evaluate

206 niche interaction and determines the fate of HSCs.

207 lls becoming highly motile and a fraction of HSCs expanding clonally within spatially restricted doma

208 GFI1B have roles in altering the function of HSCs to confer disease risk.

209 ~20 years of added proliferative history of HSCs in recipients compared with their donors, with telo

210 on of markers of fibrogenesis; incubation of HSCs with 3PO or knockdown of PFKFB3 reduced their activ

211 The majority of HSCs showed a dynamic non-spherical morphology and signi

212 ely feasible because of the large numbers of HSCs required.

213 , at least in part because of the paucity of HSCs and the modest ex vivo expansion of HSCs in media t

214 pigenetic but not transcriptional priming of HSCs/MPPs prior to their lineage commitment.

215 future to improve the in vitro production of HSCs.

216 rgy, but the overall metabolic properties of HSCs remain elusive.

217 d homeostasis requires a dynamic response of HSCs to stress, and dysregulation of these adaptive-resp

218 C behaviour, given that the visualization of HSCs in the native niche in live animals has not, to our

219 to prospectively isolate chronologically old HSCs with transcriptional features and functional attrib

220 that MMP is a source of heterogeneity in old HSCs, and its pharmacological manipulation can alter tra

221 ndispensable for Cdc42-dependent activity on HSC asymmetric division and fate.

222 showed a similar binding affinity to GRPR on HSC-3 cells.

223 The effect of neratinib on HSC was evaluated in transforming growth factor (TGF-bet

224 via the niche(3,4,6), CGRP acts directly on HSCs via receptor activity modifying protein 1 (RAMP1) a

225 DNMT3A that enable them to outcompete other HSCs and increase leukemia risk.

226 gnificantly expands our understanding of pre-HSC ontogeny.

227 pulation of prehematopoietic stem cells (pre-HSCs), fetal liver HSCs, and adult bone marrow HSCs.

228 precursors of hematopoietic stem cells (pre-HSCs).

229 ice, and loss of miR-146a promoted premature HSC aging and inflammation in young miR-146a-null mice,

230 3PO immediately after the surgery prevented HSC activation and reduced the severity of liver fibrosi

231 ion or knockdown of CPEB4 or PFKFB3 prevents HSC activation and fibrogenesis in livers of mice.

232 e competitive repopulation ability of primed HSCs.

233 fter four divisions, but show that primitive HSCs of adult mice continue to cycle rarely.

234 ion potential, and epigenetic state to probe HSC function and population structure, we found that los

235 rate that FBP1-deficient hepatocytes promote HSC activation by releasing HMGB1; blocking its release

236 signaling pathways that converge to promote HSC emergence predominantly in the ventral domain of the

237 on of epidermal growth factor (EGF) promoted HSC DNA repair and rapid hematologic recovery in chemoth

238 These studies demonstrate that EGF promotes HSC DNA repair and hematopoietic regeneration in vivo vi

239 In this study, we comprehensively quantified HSC localization with up to 4 simultaneous (9 total) BM

240 Quiescent HSCs are thought to rely on glycolysis for their energy,

241 ion (ERAD) governs the function of quiescent HSCs.

242 eted a subpopulation of primitive, quiescent HSCs.

243 We found that primed, but not quiescent, HSCs relied readily on glycolysis.

244 ling of human HSC microRNAs with that of rat HSC so as to identify those molecules that are conserved

245 xpression during transdifferentiation of rat HSC, however only 17 underwent changes that were conserv

246 Culture-activated rat HSCs were exposed to 0-100 ng/mL of LPS or its active co

247 ation of lymphoid progenitors and rebalanced HSC lineage output in transplantation assays.

248 Unlike sympathetic nerves, which regulate HSCs indirectly via the niche(3,4,6), CGRP acts directly

249 factor Snai2 (also known as Slug) regulated HSCs autonomously.

250 (2020) provide evidence that APA regulates HSC self-renewal and multi-potency by affecting stem cel

251 cellular and molecular mechanisms regulating HSC behaviour with the functional dysregulation of these

252 vitro propagation of long-term repopulating HSCs by preventing differentiation.

253 that the expansion of long-term repopulating HSCs was accompanied by synchronized expansion and matur

254 racterizes functional long-term repopulating HSCs.

255 mette-Guerin (BCG) or beta-glucan reprograms HSCs in the bone marrow (BM) via a type II interferon (I

256 t, unlike BCG or beta-glucan, Mtb reprograms HSCs via an IFN-I response that suppresses myelopoiesis

257 ssion or inhibition of p38 signaling rescued HSC quiescence and prevented DNA damage accumulation.

258 tantly, inhibition of mTOR, or Rheb, rescues HSC defects in Sel1L knockout mice.

259 Taken together, LSD1 and CoREST restrict HSC expansion and are principal targets of UM171, formin

260 n when translating data obtained from rodent HSC to events occurring in human cells.

261 Depleting senescent HSCs by 'senolytic' treatment with dasatinib/quercetin o

262 sponse within the BM, leading to significant HSC dysfunction including loss of engraftment ability an

263 tipotent progenitors and, occasionally, some HSCs gave rise to megakaryocytic-erythroid or myeloid pr

264 ures of human hepatoma and hepatic stellate (HSCs) cells were exposed to free fatty acids (FFAs) alon

265 f robust differentiation without substantial HSC expansion during the first week.

266 Targeting Diaph1 or Rab5a suppressed HSC activation and limited tumor growth in a tumor impla

267 imary transplantation and improved long-term HSC function at secondary transplantation.

268 to a subset of the most quiescent long-term HSCs (LT-HSCs) and that is compatible with current intra

269 vealed decreased HSC signatures in long-term HSCs from the Hopx(-/-) mice.

270 ith the rescue of the functional pool of th3 HSCs by correcting HSC-niche cross talk.

271 (2020) demonstrate that HSCs achieve this by regulating mitochondrial fission an

272 We report that HSCs in thalassemic mice (th3) have an impaired function

273 iew is based largely on studies showing that HSCs from aged mice exhibit these lineage biases followi

274 The HSC self-renewal defect is rescued after cell transplant

275 IL6, and IL8 in gingival fibroblasts and the HSC-2 cell line.

276 f UM171, forming a mechanistic basis for the HSC-promoting activity of UM171.

277 r, despite extensive characterization of the HSC state in the adult bone marrow and embryonic fetal l

278 entification of factors that can protect the HSC niche during an injury could offer a significant the

279 sympathetic nerves are known to regulate the HSC niche(3-6), the contribution of nociceptive neurons

280 Here, we show the HSC gene expression program is biased toward myelopoiesi

281 tivates p53, which substantially shrinks the HSC clonal repertoire in hematochimeric mice, although e

282 is reprogrammed upon infection, whereby the HSC compartment turns over substantially faster than at

283 nally validated the sorting strategy for the HSCs/MPPs and achieved around 90% enrichment.

284 This HSC-centric view is based largely on studies showing tha

285 molecular alterations reported in FA lead to HSC exhaustion remains poorly understood.

286 hematopoietic stem cells (HSCs), leading to HSC depletion and dysfunction and the risk of malignant

287 e marrow niche; how to apply this process to HSC maintenance and expansion has yet to be explored.

288 ich DNMT3A loss confers increased fitness to HSCs by analyzing a rare experiment of nature.

289 The total HSC population was increased, while the long-term (LT) p

290 This transient HSC-like population decreased as differentiation proceed

291 le kinetics and fate choices of transplanted HSCs in myeloablated recipients at early stage, with imp

292 but conditioned supernatant of DMOG-treated HSC induced VEGF-dependent proliferation of LSEC.

293 To understand HSC-niche interactions in altered nonmalignant homeostas

294 reporter assays and analysis in the ex vivo HSC assays.

295 and discusses important advances in ex vivo HSC expansion that are providing new biological insights

296 In vivo, HSCs were activated by repeated CCl(4) administration to

297 Cholangiocytes expressed GalR1, whereas HSCs and hepatocytes expressed GalR2.

298 s instigate the profibrogenic crosstalk with HSC and macrophages, including the reactivation of devel

299 e been reported to physically associate with HSCs.

300 unctional attributes characteristic of young HSCs, including a high rate of transcription and balance