ライフサイエンスコーパス: LSEC

1 LSEC demonstrated a high capacity for Ag uptake in vitro

2 LSEC efficiently incorporated (111)Indium and DiI-Ac-LDL

3 LSEC have unique morphology with small nanopores (50-300

4 LSEC label-retaining cells and progenitors were identifi

5 LSEC secrete factors that promote HCV infection and tran

6 LSEC VCAM-1 expression was upregulated by palmitate trea

7 LSEC-restricted deletion of Gata4 caused transformation

8 LSECs also play a key role in liver disease, as dysregul

9 LSECs and hepatocytes contained comparable numbers of fV

10 LSECs and midzonal hepatocytes were the most responsive

11 LSECs are a unique population of endothelial cells withi

12 LSECs are highly fenestrated cells; they contain transce

13 LSECs are involved in induction of immune tolerance, but

14 LSECs are specialized hepatic endothelial cells that reg

15 LSECs block adaptive immunogenic responses to Ag and ind

16 LSECs expressed functional retinal dehydrogenases and co

17 LSECs from Bmp9-KO mice also lost the expression of seve

18 LSECs from Bmp9-KO mice had a significantly reduced numb

19 LSECs secreted active fVIII into the culture medium.

20 In addition, LSECs gain enhanced capacity to capture Ag and induce T

21 Additionally, LSECs potentially are targets for a fVIII transgene duri

22 found luminal localization of PLVAP in adult LSEC using several imaging techniques.

23 wth factor receptor 2), whereas in the adult LSEC (fenestrations without diaphragms) these complexes

24 methylnitrosamine; within 5 days, 40% of all LSECs came from engrafted BM SPCs.

25 ortions, hepatocytes (parenchymal cells) and LSEC (non-parenchymal cells).

26 Proliferation of HC, HSC and LSEC was determined under DMOG in vitro.

27 prevented by RNase L activity in both KC and LSEC but not in hepatocytes.

28 were observed for the two viruses in KC and LSEC from RNase L(-/-) mice, demonstrating that both use

29 to NS2(H126R) These data suggest that KC and LSEC prevent viral spread into the parenchyma, preventin

30 and progenitors were identified in liver and LSEC progenitors in BM.

31 d, n=10/group) to assess biodistribution and LSECs phenotype.

32 f new communication hubs connecting CECs and LSECs included the hepatocyte growth factor (Hgf)/c-Met

33 The numbers of Kupffer cells and LSECs, the level of clotting factor X, and hepatocyte in

34 EG-based NP interaction with macrophages and LSECs, but also that these NPs can reduce pro-inflammato

35 udies of subcellular ultrastructures such as LSEC fenestrations.

36 rmation of fenestration after engraftment as LSECs, and exacerbated dimethylnitrosamine injury.

37 thylnitrosamine, repopulated the sinusoid as LSECs and reduced liver injury.

38 erived factors modify the cross-talk between LSECs and CECs via the HGF/c-MET axis.

39 BM LSEC progenitors did not contribute to normal LSEC turno

40 quarter of the LSECs were BM derived, and BM LSEC progenitors differentiated into fenestrated LSECs.

41 the relative contribution of resident and BM LSEC progenitors.

42 blish in rats whether liver injury causes BM LSEC progenitor cells to engraft in the liver and provid

43 However, after partial hepatectomy, BM LSEC progenitor proliferation and mobilization to the ci

44 esent in liver and BM, and recruitment of BM LSEC progenitors is necessary for normal liver regenerat

45 in recovery from partial hepatectomy than BM LSEC progenitors, but, when infused after injury, these

46 Further analysis revealed that BM LSEC progenitors expressed substantially more HGF and we

47 CC chemokine receptor 9 (CCR9) expression by LSEC-primed CD4(+) T cells.

48 hanosensitive angiocrine signals released by LSECs which promote PHTN by recruiting sinusoidal neutro

49 fr1 appears to contribute to iron sensing by LSECs, mostly under low iron conditions.

50 promote HSC quiescence and why "capillarized LSECs" lose control of HSC activation.

51 expected; liver sinusoidal endothelial cell (LSEC) depletion reduced PL liver localization but surpri

52 , lack of liver sinusoidal endothelial cell (LSEC) fenestration, and formation of an organized baseme

53 Liver sinusoidal endothelial cell (LSEC)-selective Cre deleter line, Stab2-iCreF3 , was cro

54 ons into liver sinusoidal endothelial cells (LSEC) and continuous endothelial cells (CEC) through his

55 ed mouse liver sinusoidal endothelial cells (LSEC) and examined cell biodistributions in animals.

56 ted with liver sinusoidal endothelial cells (LSEC) and only approximately 25% with KC.

57 essed on liver sinusoidal endothelial cells (LSEC) and that the liver is the major site of small immu

58 Liver sinusoidal endothelial cells (LSEC) are identified as an important source of CXCL expr

59 ved that liver sinusoidal endothelial cells (LSEC) derived from ethanol-fed rats showed several fold

60 Liver sinusoidal endothelial cells (LSEC) have been reported to express MHC class II, CD80,

61 PLVAP in liver sinusoidal endothelial cells (LSEC) have remained controversial.

62 HSC) and liver sinusoidal endothelial cells (LSEC) in accelerated liver growth.

63 tes with liver sinusoidal endothelial cells (LSEC) significantly increases the ability of hepatocytes

64 cells by liver sinusoidal endothelial cells (LSEC) supported migration into gut and gut-associated ly

65 and the liver sinusoidal endothelial cells (LSEC) which line the sinusoids activate RNase L in respo

66 g hepatocytes, sinusoidal endothelial cells (LSEC), Kupffer cells, and biliary epithelial cells.

67 fied the liver sinusoidal endothelial cells (LSEC), marked by FcgammaRIIb, as the cell within the liv

68 ngly, in liver sinusoidal endothelial cells (LSEC), the cells that form a barrier between blood and l

69 ology of liver sinusoidal endothelial cells (LSEC).

70 Liver sinusoidal endothelial cells (LSECs) act as a filter between blood and the hepatocytes

71 strae of liver sinusoidal endothelial cells (LSECs) allow passive transport of solutes, macromolecule

72 such as liver sinusoidal endothelial cells (LSECs) and hepatic stellate cells (HSCs), are the first

73 f murine liver sinusoidal endothelial cells (LSECs) and hepatocytes, but not Kupffer cells.

74 n to the liver sinusoidal endothelial cells (LSECs) are key elements in nonalcoholic steatohepatitis

75 hich rat liver sinusoidal endothelial cells (LSECs) are repopulated in the reperfused transplanted li

76 (HGF) in liver sinusoidal endothelial cells (LSECs) are thought to drive liver regeneration.

77 Liver sinusoidal endothelial cells (LSECs) are unique organ-resident APCs capable of Ag cros

78 Liver sinusoidal endothelial cells (LSECs) are uniquely differentiated to fulfill important

79 primary liver sinusoidal endothelial cells (LSECs) both revealed that the expression of the LSEC-spe

80 ets with liver sinusoidal endothelial cells (LSECs) by immunohistochemistry.

81 ate that liver sinusoidal endothelial cells (LSECs) constitute a unique population of phenotypically

82 Liver sinusoidal endothelial cells (LSECs) defenestrate and capillarize in response to aging

83 rized by liver sinusoidal endothelial cells (LSECs) defenestration extracellular matrix and glycocaly

84 Liver sinusoidal endothelial cells (LSECs) differ, both structurally and functionally, from

85 Liver sinusoidal endothelial cells (LSECs) have long been noted to contribute to liver regen

86 re the role of sinusoidal endothelial cells (LSECs) in the adult liver, we studied the effects of vas

87 duced by liver sinusoidal endothelial cells (LSECs) into pressure and matrix changes.

88 Liver sinusoidal endothelial cells (LSECs) make up a large proportion of the nonparenchymal

89 Normal liver sinusoidal endothelial cells (LSECs) promote quiescence of hepatic stellate cells (HSC

90 r cells, liver sinusoidal endothelial cells (LSECs), hepatocytes, scavenger receptors, clotting facto

91 ected in liver sinusoidal endothelial cells (LSECs), monocytes, and Kupffer cells, whereas combinator

92 ation of liver sinusoidal endothelial cells (LSECs), precedes the onset of hepatic fibrosis.

93 (FVIII)-liver sinusoidal endothelial cells (LSECs)-can improve the outcome of hemophilia A (HA) gene

94 usoid as liver sinusoidal endothelial cells (LSECs).

95 aling in liver sinusoidal endothelial cells (LSECs).

96 ance are liver sinusoidal endothelial cells (LSECs).

97 Cs), and liver sinusoidal endothelial cells (LSECs).

98 BMP6) in liver sinusoidal endothelial cells (LSECs).

99 ADCs by liver sinusoidal endothelial cells (LSECs).

100 itors of liver sinusoidal endothelial cells (LSECs, also called sinusoidal endothelial cell progenito

101 ene dysregulation was analyzed in primary CH-LSECs and liver tissues from rats and humans with cirrho

102 GGTA1, CMAH LSECs exhibited reduced levels of human platelet binding

103 VIII activity and AcLOL uptake in cocultured LSECs through the production of short-range paracrine si

104 In conclusion, LSEC progenitor cells are present in liver and BM, and r

105 Under certain conditions, LSECs can switch from a tolerogenic to an immunogenic st

106 By contrast, LSECs respond efficiently to TGFB1 treatment, which caus

107 regulator of liver homeostasis, controlling LSEC fenestration and protecting against perivascular he

108 , in the absence of exogenous costimulation, LSEC induced negligible proliferation of CD4(+) or CD8(+

109 rat cirrhotic liver tissue, as well as in CT-LSEC treated with miR-153-3p-hepEVs, indicating enhanced

110 ats and humans with cirrhosis, as well as CT-LSECs treated with miRNA-specific upregulated hepEVs.

111 However, unlike DC, LSEC had low or absent expression of MHC class II, CD86,

112 ss of fenestrae that result in defenestrated LSECs.

113 Lack of maturation of BM-derived LSECs is due to cell autonomous pathways that inhibit th

114 unctional engraftment of bone marrow-derived LSECs after cold ischemia and warm reperfusion.

115 are necessary to maintain the differentiated LSEC phenotype.

116 nother main characteristic of differentiated LSECs is the presence of permeable fenestrae.

117 The switch from discontinuous LSECs to continuous ECs during embryogenesis caused live

118 pecifically transduced liver sinusoidal ECs (LSECs) but not Kupffer cells, which were mainly transduc

119 continuous cell layer, liver sinusoidal ECs (LSECs) constitute discontinuous, permeable microvessels.

120 Herein, we report that liver sinusoidal ECs (LSECs; defined as CD146(+)CD45(-)) exhibit increased int

121 For example, in contrast to other ECs, LSECs possess fenestrations, have low detectable levels

122 , NPCs-Kupffer (KC), sinusoidal endothelial (LSEC) and stellate cells (SC) are major cellular compone

123 Moreover, IFNalpha endowed LSECs with efficient cross-priming potential that, along

124 By using magnetically enriched LSEC (CD146(+)) populations, we show evidence of marked

125 progenitors differentiated into fenestrated LSECs.

126 Nevertheless, PLVAP in fetal LSEC (fenestrations with diaphragms) associated with LYV

127 n of T regulatory cells, in hepatic fibrosis LSECs induce an immunogenic T cell phenotype capable of

128 unlike LSECs in normal livers, in fibrosis, LSECs do not veto dendritic cell priming of T cells.

129 Prior to fibrosis, LSECs undergo capillarization, which is permissive for H

130 sing electron microscopy on chemically fixed LSECs.

131 These studies identify a role for LSEC and BMP4 in HCV infection and highlight BMP4 as a n

132 m the enriched nonparenchymal cell fraction, LSEC (CD45(-)) were then isolated to 99% purity using im

133 as an organ-specific angiokine derived from LSECs.

134 as BMP2, BMP6, and TGFB1, are released from LSECs and signal in a paracrine manner to hepatocytes an

135 f bone marrow-derived cells into functioning LSECs is routinely between 1% and 5%.

136 Further, LSEC were treated with cytochalasin B to demonstrate the

137 crossed with Acvrl1 -floxed mice to generate LSEC-specific Acvrl1 -deficient mice ( Alk1HEC-KO ).

138 ter fibrotic liver injury from hepatotoxins, LSECs become highly proinflammatory and secrete an array

139 on of inductive VEGFR2(+)Id1(+)Wnt2(+)HGF(+) LSECs with hepatocytes provides an effective strategy to

140 ced with Wnt2 and HGF (Id1(-/-)Wnt2(+)HGF(+) LSECs) re-establishes an inductive vascular niche in the

141 ding to capillarization and to determine how LSECs promote HSC quiescence and why "capillarized LSECs

142 or (huCD105-LV) transduced exclusively human LSECs in mice transplanted with human liver ECs.

143 Primary human LSECs (HLSECs) and immortalized liver endothelial cells

144 enic transplantation of Id1(+/+) or Id1(-/-) LSECs transduced with Wnt2 and HGF (Id1(-/-)Wnt2(+)HGF(+

145 Most importantly, we have identified LSEC FcyRIIb-mediated endocytosis to be the Fc effector

146 ntains HSC quiescence and show that immature LSECs are unable to shed HB-EGF from the cytosolic membr

147 In LSEC in vitro , stimulation or inhibition of ALK1 signal

148 known PLVAP-dependent molecular complexes in LSEC during angiogenesis.

149 over, most (90%) liver RIIb was expressed in LSEC, the remainder in Kupffer cells.

150 al time PCR we found messenger expression in LSEC to be about 5 times higher than in hepatocytes.

151 An absent FcRgamma in LSEC implied that RIIb is the sole FcgammaR expressed.

152 Here we show that fenestrations in LSEC contain PLVAP-diaphragms during the fetal angiogene

153 on and elucidated the mechanisms involved in LSEC-induced T cell immunity.

154 vitro co-cultures, VEGFR2-Id1 activation in LSECs stimulates hepatocyte proliferation.

155 EGFR2-Id1-mediated inductive angiogenesis in LSECs through release of angiocrine factors Wnt2 and HGF

156 the liver, we conditionally deleted Bmp2 in LSECs using EC subtype-specific Stab2-Cre mice.

157 orming centers and defenestration centers in LSECs under different experimental conditions.

158 vivo, hepEVs-CH accumulated predominantly in LSECs, disrupting genes involved in fibrosis, inflammati

159 Disruption of Notch1 signaling in LSECs leads to spontaneous formation of angiosarcoma, in

160 nctionally interlinked with BMP signaling in LSECs, suggesting druggable targets for the treatment of

161 After intraportal injection, LSEC were largely in the liver (60 +/- 13%) and, after s

162 [sprocs]) with diminished repair of injured LSECs and whether restoring signaling to recruit BM spro

163 capillarization is due to repair of injured LSECs by BM endothelial progenitors that engraft but fai

164 ing to recruit BM sprocs that repair injured LSECs renders steatotic liver more susceptible to I/R in

165 merging data suggest that even after injury, LSEC expression of HGF does not increase greatly.

166 r-dimensional AFM (X, Y, Z, and t) on intact LSECs in vitro.

167 Likewise, LSEC VCAM-1 expression was reduced in the Mlk3-/- mice w

168 Furthermore, whereas in normal livers, LSECs are active in the generation of T regulatory cells

169 the latest advances in AFM imaging on living LSECs.

170 rast to endothelial progenitor cells, mature LSECs express little HGF.

171 n recruited to the liver, rather than mature LSECs, drive liver regeneration.

172 a critical role for death receptor-mediated LSEC injury and show the first evidence that Kupffer cel

173 Moreover, LSEC VCAM-1 expression was significantly increased in hu

174 e spleen (29 +/- 10%; P < .01), whereas most LSEC migrated to the liver or lungs.

175 e transcription factor GATA4 controls murine LSEC specification and function.

176 ncogenic hepatocyte senescence drives murine LSEC NF-kappaB activity in vivo.

177 compare the phenotype and function of murine LSEC and DC.

178 Exposure of murine LSEC primary cultures to these ligands shows that autocr

179 SEC progenitors did not contribute to normal LSEC turnover in the liver.

180 As aging occurs, LSECs have a reduction in both the number and size of fe

181 n of BMP4 abrogated the proviral activity of LSEC-conditioned media.

182 Flow cytometric analysis of LSEC demonstrated high expression of CD31, von Willebran

183 These findings may facilitate analysis of LSEC for cell and gene therapy applications.

184 lopment of liver fibrosis and the changes of LSEC phenotype occur in the early stage of liver fibrosi

185 e life span, formation, and disappearance of LSEC fenestrae; by doing so, we also gathered evidence o

186 d these cells to the promigratory effects of LSEC-derived Hgf.

187 lipotoxic stress enhances the expression of LSEC VCAM-1, in part, through MLK3 signaling.

188 eneration, owing to diminished expression of LSEC-derived angiocrine factors, including hepatocyte gr

189 been purported to be a specific function of LSEC, we found DC captured acetylated low-density lipopr

190 ion of both SE-1 and phenotypic functions of LSEC such as factor VIII activity and AcLOL uptake in co

191 egeneration was compromised, but infusion of LSEC progenitors rescued the defect.

192 Loss of LSEC angiokines Wnt2 , Wnt9b , and R-spondin-3 ( Rspo3 )

193 d with poor clinical outcome and the loss of LSEC marker gene expression.

194 Maintenance of LSEC differentiation requires vascular endothelial growt

195 The effector mechanism of LSEC FcyRIIb was identified to be endocytosis.

196 cell deficiency did not reverse the onset of LSEC apoptosis/damage.

197 tion of KC by gadolinium(III) chloride or of LSEC by cyclophosphamide partially restores liver replic

198 results lead us to propose a new paradigm of LSEC and HDL in clearing LPS with a potential to avoid i

199 HSC induced VEGF-dependent proliferation of LSEC.

200 Notably, the ratio of LSEC-KC-associated LPS remained unchanged 45 min after i

201 Restoration of LSEC differentiation in vivo promotes HSC quiescence, en

202 We investigated whether restoration of LSEC differentiation would normalize crosstalk with acti

203 sinusoids improved intrahepatic retention of LSEC to 89 +/- 7% and 89 +/- 5%, respectively (P < .01).

204 lated that, in liver fibrosis, a reversal of LSEC function from tolerogenic to proinflammatory and im

205 Thus, we proposed that RIIb of LSEC eliminates blood-borne SIC, thereby controlling imm

206 The state of LSEC differentiation plays a pivotal role in HSC activat

207 In conclusion, the targeting of LSEC to the liver and other organs is directed by vascul

208 howed robust transcriptional upregulation of LSEC VCAM-1 in murine NASH.

209 C-associated transcripts and upregulation of LSEC-associated genes.

210 al properties of the filtration apparatus of LSECs.

211 In contrast, bone marrow progenitor cells of LSECs (BM SPCs), which are rich in HGF, are recruited to

212 that addition of BMP9 to primary cultures of LSECs prevented the loss of their fenestrae and maintain

213 Primary cultures of LSECs were established in which fVIII mRNA levels were i

214 ylnitrosamine caused extensive denudation of LSECs at 24 hours, followed by centrilobular hemorrhagic

215 Moreover, depletion of LSECs from fibrotic liver cultures mitigates the proinfl

216 maintains quiescence and differentiation of LSECs in adult mice.

217 capillarization (restored differentiation of LSECs) without directly affecting activation of HSCs or

218 basic structure of LSECs, and the effect of LSECs on hepatic inflammation and fibrosis during aging

219 for intestinal DCs but is also a feature of LSECs.

220 PL incubations; conversely, the intensity of LSECs was higher after PL incubations than with CNP incu

221 We found that the majority of LSECs in livers cold-stored for 18 hours in University o

222 nvestigated whether functional maturation of LSECs can be achieved by TLR ligand stimulation and eluc

223 ver, little is known about the mechanisms of LSECs to induce T cell immunity.

224 We demonstrate that pretreatment of LSECs with palmitoyl-3-cysteine-serine-lysine-4 (P3C; TL

225 c liver injury can recruit BM progenitors of LSECs that engraft and fail to fully differentiate, whic

226 th a persistent increase in proliferation of LSECs.

227 uced tumorigenesis, a gradual replacement of LSECs by CECs was associated with dynamic changes in the

228 ffer a critical understanding of the role of LSECs in modulating intrahepatic immunity and inflammati

229 RNA-sequencing of LSECs identified proteins in mechanosensitive signaling

230 ulation and that the immunological status of LSECs was dependent upon the balance between programmed

231 Mechanical stretch of LSECs increased expression of CXCL1 via integrin-depende

232 review, we described the basic structure of LSECs, and the effect of LSECs on hepatic inflammation a

233 In studies of LSECs and knockout mice, we identified mechanosensitive

234 early stage of liver fibrosis, the study of LSECs in the fibrotic liver is valuable for the detectio

235 ffer cells are essential to the viability of LSECs, which appears to be mediated through glycoprotein

236 ion of alpha(4) beta(7) integrin and CCR9 on LSEC-primed CD4(+) T cells, consequently reducing their

237 V/fibronectin as having a positive effect on LSEC survival.

238 RIIb on LSEC, a major scavenger, keeps SIC blood concentrations

239 We found that S1P(1) was enriched on LSECs in vivo and in primary cell culture and that VPC23

240 a decrease in glycoprotein 130 expression on LSECs, suggesting that STAT3 activation may protect thes

241 duce programmed death ligand 1 expression on LSECs, thereby favoring T cell proliferation and activat

242 Second, the SASP up-regulates ICOSLG on LSECs, with the ICOS-ICOSLG axis contributing to senesce

243 to cross-contamination in the hepatocyte or LSEC preparations.

244 suggest that during systemic iron overload, LSECs internalize NTBI, which promotes oxidative stress

245 mulation of both angiogenesis and pathogenic LSEC capillarization, as well as demonstrating a role fo

246 Consistent with their phenotype, LSEC were poor stimulators of allogeneic T cells.

247 aused functional maturation of Ag-presenting LSECs and enabled them to activate virus-specific CD8(+)

248 attractant CXCL1 was up-regulated in primary LSECs exposed to mechanical stretch, compared with unexp

249 We isolated primary LSECs from mice and induced mechanical stretch with a Fl

250 hought to increase markedly in proliferating LSECs.

251 levels were indistinguishable from purified LSECs.

252 Use of radiolabeled LSEC showed differences in cell biodistributions in rela

253 In further studies using radiolabeled LSEC, we established that the manipulation of receptor-m

254 ory cytochemokines compared with control rat LSEC.

255 ally, ethanol-induced ET-1 expression in rat LSEC is regulated by miR-199, while in human endothelial

256 Rat LSECs were cultured with inhibitors and/or agonists and

257 ge vessel endothelial cells and repopulating LSECs.

258 Resident LSEC progenitors within their niche may play a smaller r

259 GF and were more proliferative than resident LSEC progenitors after partial hepatectomy.

260 of this pathway downstream from NO restores LSEC differentiation in vivo.

261 tion of CYSLTR1 and GPBAR1 potently reversed LSEC/monocyte interactions.

262 Since LSECs play an important role in the development of liver

263 ver, after intrasplenic injection, only some LSEC remained in the spleen (29 +/- 10%; P < .01), where

264 We applied 3D-SIM to multi-color stained LSECs to acquire highly resolved overviews of large samp

265 -phosphate-stimulated and arsenic-stimulated LSEC oxidant generation and defenestration.

266 on of SR-B1 by flow cytometry, we found that LSEC expressed considerable amounts of SR-B1 while in he

267 to previous reports, our data indicate that LSEC alone are insufficient to activate naive T cells.

268 anged 45 min after infusion, indicating that LSEC independently processes the LPS.

269 We find that LSECs induce the hepatic expression of the LDL receptor

270 Our data suggest that LSECs undergo maturation exclusively in response to TLR1

271 The LSEC-mediated CD8(+) T cell immunity was initiated by so

272 cs and informatics were used to identify the LSEC mediator that maintains HSC quiescence.

273 A for factor IX, a hepatocyte marker, in the LSEC preparation, nor was there detectable mRNA for von

274 nd elicited more profound alterations in the LSEC transcriptome than holo-transferrin injection.

275 Thus, dysregulation of the LSEC phenotype is a critical step in the fibrotic proces

276 th factor (HGF) was identified as one of the LSEC-derived paracrine mediators promoting hepatocyte gr

277 Cs) both revealed that the expression of the LSEC-specifying transcription factor GATA-binding protei

278 ellular matrix and neighboring cells, on the LSEC phenotype in vitro.

279 h factor (VEGF)-A receptor-2 (VEGFR2) in the LSECs impairs the initial burst of hepatocyte proliferat

280 characterized distinct subpopulations of the LSECs themselves with a high resolution and defined thei

281 In the liver, one-quarter of the LSECs were BM derived, and BM LSEC progenitors different

282 Restoration of differentiation to LSECs led to quiescence of HSCs and regression of fibros

283 ential to induce gut homing is restricted to LSECs.

284 cent protein (GFP) expression, and tranduced LSEC with a GFP-lentiviral vector.

285 Transplanted LSEC were distinct from Kupffer cells with expression of

286 Transplanted LSEC were found in the liver, lungs, and spleen shortly

287 To identify transplanted LSEC in tissues, we labeled cells metabolically with DiI

288 ed the same results in acute ethanol-treated LSEC from control rats and human dermal microvascular en

289 ulate growth of hepatocytes in vitro, unless LSECs were also present in the culture.

290 Similarly, unlike LSECs in normal livers, in fibrosis, LSECs do not veto d

291 cles (DiI-Ac-LDL) or (111)Indium-oxine, used LSEC from Rosa26 donors expressing beta-galactosidase or

292 apoptosis, with a twofold decline in viable LSECs in CLP animals compared with sham controls.

293 However, whether LSEC-secreted factors can act in an autocrine manner to

294 ently tagged LPS-HDL complex associates with LSEC, suggesting that HDL facilitates LPS clearance.

295 oprotein (HDL)-mediated LPS association with LSEC early in the process.

296 l extracellular traps [NETs]), and mice with LSEC-specific deletion of Notch1 (Notch1(iDeltaEC)).

297 We suggest that coculture with LSECs induces the emergence of a sinusoidal surface in p

298 e particles, the hepatocytes cocultured with LSECs showed a high level of HCV-like particle uptake.

299 t incorporating primary rat hepatocytes with LSECs, SCs, and KCs.

300 ing in vitro when compared with GGTA1 and WT LSECs.