ライフサイエンスコーパス: stellate cell

1 n the overall bile acid uptake in pancreatic stellate cells.

2 ramidal cells were superimposed on scattered stellate cells.

3 asic effect on EPSC amplitudes recorded from stellate cells.

4 liver, their expansion supported by hepatic stellate cells.

5 onic stem cells, gastric tumors, and hepatic stellate cells.

6 al signaling, and Crbp1 levels in VA storing stellate cells.

7 y phenotype in pancreatic normal, cancer and stellate cells.

8 ng protein Crbp1 (RBP1) levels in VA-storing stellate cells.

9 ctivates fibrosis-related markers in hepatic stellate cells.

10 sis is limited compared with that of hepatic stellate cells.

11 onstellate principal cells (NSPCs) and in no stellate cells.

12 he microfluidic devices containing activated stellate cells.

13 4F nanoparticles were incubated with hepatic stellate cells.

14 s, sinusoidal endothelial cells, and hepatic stellate cells.

15 ely rescues teashirt loss of expression from stellate cells.

16 to be ~4 for rat basket cells and ~1 for rat stellate cells.

17 ell as primary human hepatocytes and hepatic stellate cells.

18 s marker activation in primary human hepatic stellate cells.

19 (+) -dependent bile acid uptake mechanism in stellate cells.

20 only signalling in acinar cells but also in stellate cells.

21 e tracing to follow transplanted rat hepatic stellate cells, a resident liver mesenchymal cell popula

22 In stellate cells, a voltage-dependent increase in membrane

23 y liver disease activity scores, and hepatic stellate cell activation (alpha-smooth muscle actin) com

24 ic alphaSMA expression, a marker for hepatic stellate cell activation (r = -0.31, P < 0.02).

25 enefitted liver fibrosis via altered hepatic stellate cell activation and extracellular matrix remode

26 cided with alterations in markers of hepatic stellate cell activation and extracellular matrix remode

27 Estrogens inhibit stellate cell activation and fibrogenesis.

28 fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis.

29 he activity of the PAR2 pepducin on cultured stellate cell activation and hepatocyte reactive oxygen

30 he dKO mice had similar levels of markers of stellate cell activation and matrix remodeling as Ppara(

31 usoidal endothelial cell capillarization and stellate cell activation demonstrates allograft injury i

32 C1QTNF2 expression is reduced during hepatic stellate cell activation in culture and in a mouse model

33 Vitamin A loss is accompanied by stellate cell activation in hepatic tissue.

34 osis and suppressed expression of markers of stellate cell activation in livers of mice fed a diet ri

35 Finally, MSDC-0602 directly reduced hepatic stellate cell activation in vitro, and MSDC-0602 treatme

36 nanoparticles were found to suppress hepatic stellate cell activation in vitro.

37 ent or hepatocyte MPC2 deletion also limited stellate cell activation indirectly by affecting secreti

38 Stellate cell activation leads to hepatic fibrosis; furt

39 FR reduced hepatic stellate cell activation markers (transforming growth fa

40 LOX inhibition attenuated hepatic stellate cell activation markers and promoted F4/80-posi

41 rentiation into polarized MPhis that mediate stellate cell activation via TGF-beta.

42 Hepatic stellate cell activation was detected by immunofluoresce

43 r sinusoidal endothelial cell activation and stellate cell activation was increased in patients with

44 tion of hepatic progenitor cell response and stellate cell activation, and normalization of liver enz

45 artly mediated through inhibition of hepatic stellate cell activation, and significant decreases in p

46 duced liver fibrosis associated with hepatic stellate cell activation, hepatitis, and liver injury.

47 Besides stellate cell activation, increased numbers of stem/prog

48 r injury; or reduce expression of markers of stellate cell activation, liver inflammation, and injury

49 l protein adducts accompanied by evidence of stellate cell activation, matrix remodeling, and fibrosi

50 iated with hepatic progenitor cell features, stellate cell activation, NOTCH signaling, and an aggres

51 iferation, senescence, fibrosis, and hepatic stellate cell activation, which were reduced in Hdc(-/-)

52 substrate stiffening resulted in attenuated stellate cell activation, with reduced YAP/TAZ nuclear s

53 amine the relationship between retinoids and stellate cell activation.

54 activity and membrane insertion in wild-type stellate cell activation.

55 ve, LD-associated protein that helps mediate stellate cell activation.

56 f inflammation, macrophage infiltration, and stellate cell activation.

57 tivation, prothrombin activation and hepatic stellate cell activation.

58 models of monocyte/macrophage and/or hepatic stellate cell activation.

59 vated monocytes/macrophages promoted hepatic stellate cell activation.

60 owever, the molecular mechanisms for hepatic stellate-cell activation by HCV-infected hepatocytes are

61 Furthermore, during licking, stellate cell activity was anisotropic: the coordination

62 Addition of hepatic stellate cells allowed generation of myeloid-derived sup

63 is not normally expressed in larval or adult stellate cells, almost completely rescues teashirt loss

64 ed by ClC-a, is exclusively expressed in the stellate cell and is required for Drosophila kinin-media

65 Smooth-muscle actin expression by stellate cells and CD34 expression by liver sinusoidal e

66 mpanied by enhanced activation of pancreatic stellate cells and elevated levels of serum retinoic aci

67 We found that Sema7A is expressed in spiny stellate cells and GABAergic interneurons and that its a

68 is an emerging new target expressed on liver stellate cells and hepatocytes that regulates the respon

69 ro experiments were performed in rat hepatic stellate cells and hepatocytes.

70 ARC is secreted at high levels by pancreatic stellate cells and is regulated by metabolic parameters

71 ression (LTD) between cortical layer 4 spiny stellate cells and layer 2/3 pyramidal cells requires th

72 We identify potent MMIC activity in hepatic stellate cells and liver sinusoidal endothelial cells.

73 ing cellular senescence in activated hepatic stellate cells and portal fibroblasts by engaging integr

74 eceptor, CD74, that is released from hepatic stellate cells and that binds MIF, neutralizing its sign

75 in [Ca](o) on the excitability of cerebellar stellate cells and their inhibitory regulation of Purkin

76 r escalated by bradykinin-induced signals in stellate cells and thus killing of stellate cells by bil

77 rosis in a yin-yang interaction with hepatic stellate cells, and are a key component of tumor-promoti

78 es in the majority of pyramidal cells, spiny stellate cells, and interneurons within the extrastriate

79 fibrogenic activation of attenuated hepatic stellate cells, and limits fibrosis reversal.

80 sinophils, neutrophils, macrophages, hepatic stellate cells, and lymphocytes all identified as major

81 dothelin-induced vasoconstriction by hepatic stellate cells, and not platelet accumulation or coagula

82 etwork that includes macrophages, pancreatic stellate cells, and prominent cytokines that are present

83 a subset of TGF-beta target genes in hepatic stellate cells, and the cooperation between the JAK1-STA

84 Hepatic stellate cells are liver-specific mesenchymal cells that

85 Activated hepatic stellate cells are the main source of excessive collagen

86 cinar cells but the effects of bile acids on stellate cells are unexplored.

87 ted excitatory synaptic responses, which, in stellate cells, are largely extrasynaptic, without a cha

88 Barrel cortex layer IV spiny stellate cells (bSCs) are the primary recipients of asce

89 in CAF and in myofibroblastic human hepatic stellate cells but lacked similar effects in quiescent f

90 companied by increased activation of hepatic stellate cells, but hepatic mediators of inflammation we

91 ces Bmp6 mRNA expression in isolated hepatic stellate cells, but not in hepatocytes.

92 xposure decreased Sirt1 and Timp3 in hepatic stellate cells by a NOX2-dependent pathway, and TACE was

93 ignals in stellate cells and thus killing of stellate cells by bile acids might have important implic

94 oid and cholesterol metabolism are linked in stellate cells by the LD-associated protein Rab18.

95 Early postnatally, layer-2 pyramidal but not stellate-cells co-localized with doublecortin - a marker

96 more dramatic Ca(2+) signals and necrosis in stellate cells compared to the adjacent acinar cells in

97 n situ liver perfusion system and on hepatic stellate cell contraction in vitro.

98 wn to reside in the principal cells, whereas stellate cells control the anion conductance, but by an

99 on of miR-200b in cholangiocytes and hepatic stellate cells decreased the expression of miR-200b, ang

100 e, reduces asymmetrical orientation of spiny stellate cell dendrites, and functionally impairs thalam

101 flammation accompanied with elevated hepatic stellate cell-derived TnC and Toll-like receptor 4 expre

102 ivation of the autophagic pathway in hepatic stellate cells during Brucella infection could have an i

103 tes in lung myofibrogenesis as suggested for stellate cells during liver fibrosis.

104 ities of hepatocytes, Kupffer cells, hepatic stellate cells, endothelial cells, and circulating immun

105 rikingly, electrophysiological recordings in stellate cells from these PV-Cre/NL123 cKO mice revealed

106 For cerebellar granule cell to stellate cell (grc-->SC) synapses, AAV1 also led to arti

107 ), which is secreted by activated pancreatic stellate cells, has important functions in chronic pancr

108 poptosis resistance in primary human hepatic stellate cells (hHSC).

109 anscriptome of rat PMFs, compared to hepatic stellate cell HSC-derived myofibroblasts in culture, ide

110 he role of inflammatory mediators in hepatic stellate cell (HSC) activation and HSC survival during f

111 receptors (LXRs) are determinants of hepatic stellate cell (HSC) activation and liver fibrosis.

112 yrosine kinases, which contribute to hepatic stellate cell (HSC) activation and liver fibrosis.

113 Hepatic stellate cell (HSC) activation and transforming growth f

114 Hepatic stellate cell (HSC) activation on liver injury facilitat

115 ncreased after pIVCL concurrent with hepatic stellate cell (HSC) activation.

116 merase chain reaction for markers of hepatic stellate cell (HSC) activation.

117 extracellular matrix components and hepatic stellate cell (HSC) activation.

118 h enhances TGF-beta signaling during hepatic stellate cell (HSC) activation.

119 ed as an immediate-early gene during hepatic stellate cell (HSC) activation.

120 ould partly account for reduction of hepatic stellate cell (HSC) activation.

121 Mphi and IL-34-Mphi also express the hepatic stellate cell (HSC) activators, platelet-derived growth

122 nd the molecular mediators of EMT in hepatic stellate cell (HSC) and human liver cancer cells (HepG2)

123 on, LPC biliary differentiation, and hepatic stellate cell (HSC) chemotaxis.

124 4 (CXCR4) pathway directly promotes hepatic stellate cell (HSC) differentiation and activation throu

125 beta-4 (TB4) involved in regulating hepatic stellate cell (HSC) functions remain unclear.

126 Hepatic stellate cell (HSC) transdifferentiation from a quiescen

127 f extracellular matrix components by hepatic stellate cell (HSC)-derived myofibroblasts.

128 n (qRT-PCR) and western blotting and hepatic stellate cell (HSC)-MF contractility by gel contraction

129 type 2 (CCR2) is expressed by active hepatic stellate cells (HSC) and is a key monocyte recruitment s

130 inib reduced EGFR phosphorylation in hepatic stellate cells (HSC) and reduced the total number of act

131 Hepatic stellate cells (HSC) are a major source of the immunoreg

132 Hepatic stellate cells (HSC) are the major source of extracellul

133 Recently, human hepatic stellate cells (HSC) have been reported to induce monocy

134 nvolvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study.

135 iorates liver fibrosis by inhibiting hepatic stellate cells (HSC), and loss of miR-200a is associated

136 nse (UPR) both promote activation of hepatic stellate cells (HSC), however the link between the two s

137 incipally regulated by activation of hepatic stellate cells (HSC).

138 factor (CCN2) drives fibrogenesis in hepatic stellate cells (HSC).

139 (FAK) plays a key role in promoting hepatic stellate cells (HSCs) activation in vitro and liver fibr

140 cipally expressed in quiescent mouse hepatic stellate cells (HSCs) and directly suppressed production

141 Hepatic stellate cells (HSCs) and portal fibroblasts (PFs) are b

142 liver fibrosis remission by killing hepatic stellate cells (HSCs) and producing interferon (IFN)-gam

143 IL-20 activated quiescent rat hepatic stellate cells (HSCs) and up-regulated TGF-beta1 express

144 Hepatic stellate cells (HSCs) are key players in the development

145 In liver fibrogenesis, hepatic stellate cells (HSCs) are thought to transdifferentiate

146 -1alpha (HIF-1alpha) is activated in hepatic stellate cells (HSCs) by hypoxia and regulates genes imp

147 kinase receptor, is up-regulated in hepatic stellate cells (HSCs) during chronic liver injury.

148 Effects of LPS on fibrogenic hepatic stellate cells (HSCs) from WT and TLR4-KO mice were asse

149 Hepatic stellate cells (HSCs) have been identified as the main f

150 Retinoid-storing hepatic stellate cells (HSCs) have recently been described as a

151 Activation of hepatic stellate cells (HSCs) in response to injury is a key ste

152 gammadelta T cells colocalized with hepatic stellate cells (HSCs) in vivo and promoted apoptosis of

153 Hepatic stellate cells (HSCs) induce hepatic inflammation and im

154 Hepatic stellate cells (HSCs) inhibit T cells, a process that co

155 We answered the questions of whether hepatic stellate cells (HSCs) interact with CD4+ T cells during

156 Activation of hepatic stellate cells (HSCs) is a critical step in the developm

157 Activation of hepatic stellate cells (HSCs) is a key event in the initiation o

158 er disease mediated by activation of hepatic stellate cells (HSCs) leads to liver fibrosis.

159 erating cholangiocytes and activated hepatic stellate cells (HSCs) participate in the promotion of li

160 Hepatic stellate cells (HSCs) play a major role increasing IHVR

161 Hepatic stellate cells (HSCs) play critical roles in liver fibro

162 and pro-fibrogenic environment with hepatic stellate cells (HSCs) remodeling the extracellular matri

163 lls to the liver to remove activated hepatic stellate cells (HSCs) significantly and ameliorate liver

164 e demonstrated previously that mouse hepatic stellate cells (HSCs) suppress T cells via programmed de

165 rix proteins, such as collagen I, by hepatic stellate cells (HSCs) that culminates in cirrhosis.

166 hese secreted cytokines may activate hepatic stellate cells (HSCs) toward fibrosis.

167 Hepatic stellate cells (HSCs) were recently identified as liver-

168 Hepatic stellate cells (HSCs) were treated with or without adipo

169 e-transgenic mouse that marks 99% of hepatic stellate cells (HSCs), a liver-specific pericyte populat

170 increased LPA levels, activation of hepatic stellate cells (HSCs), and amplification of profibrotic

171 soidal endothelial cells (LSECs) and hepatic stellate cells (HSCs), are the first liver cells to enco

172 In cultured hepatic stellate cells (HSCs), disrupting Hedgehog signaling blo

173 s were performed with primary rodent hepatic stellate cells (HSCs), Kupffer cells (KCs), and hepatocy

174 directly targeting Gli3 in activated hepatic stellate cells (HSCs), reduces expression of Gli3 and pr

175 ophage colony-stimulating factor and hepatic stellate cells (HSCs), resulting in the generation of MD

176 transcriptome signature of activated hepatic stellate cells (HSCs), the primary collagen-secreting ce

177 eta1 recruited IQGAP1 to TbetaRII in hepatic stellate cells (HSCs), the resident liver pericytes.

178 sm of this resistance by focusing on hepatic stellate cells (HSCs), which are known to regulate Treg

179 elial neoplasia, or PDAC, as well as hepatic stellate cells (HSCs).

180 luding laminin (Ln)-332, produced by hepatic stellate cells (HSCs).

181 pecial focus on the STAT3 pathway in hepatic stellate cells (HSCs).

182 omes could regulate the phenotype of hepatic stellate cells (HSCs).

183 factor-beta (PDGFB) is a mitogen for hepatic stellate cells (HSCs).

184 Kupffer cells (KCs), neutrophils, or hepatic stellate cells (HSCs).

185 deposition of collagen by activated hepatic stellate cells (HSCs).

186 as retinyl esters in the retina and hepatic stellate cells (HSCs).

187 SEMA7A is highly expressed in hepatic stellate cells (HSCs).

188 liferation and activation of resting hepatic stellate cells (HSCs).

189 fibrosis is marked by activation of hepatic stellate cells (HSCs).

190 as more than just an alternative to hepatic stellate cells in fibrosis.

191 the organization of glutamatergic input from stellate cells in layer 2 and from the hippocampus, with

192 cellular electrophysiological properties of stellate cells in layer II of MEC change systematically

193 Stellate cells in layer II of the mEC project to the hip

194 0 was much higher in hepatocytes and hepatic stellate cells in liver biopsies from patients with fibr

195 s in acinar cells, had only minor effects on stellate cells in lobules.

196 cells (NFkappaB) in hepatocytes and hepatic stellate cells in monoculture; however, they do not acco

197 Voltage clamp recordings from mEC stellate cells in rat brain slices showed that GTx inhib

198 receive a spatially broad inhibition from D-stellate cells in the AVCN, and a spatially confined inh

199 tor function at parallel fibre synapses onto stellate cells in the cerebellum using whole-cell patch-

200 duced fibrosis and the numbers of pancreatic stellate cells in the tumor stroma and altered the types

201 e major cerebellar neuroligin isoforms, from stellate cells in triple NL123 conditional knock-out mic

202 pathophysiological effects of bile acids on stellate cells in two experimental models: ex vivo (mous

203 on of miR-200b in cholangiocytes and hepatic stellate cells in vitro, we evaluated angiogenesis and f

204 mor-derived JAG1 signaling activated hepatic stellate cells, increasing their recruitment to vasculat

205 We recently demonstrated that hepatic stellate cells induce the differentiation of myeloid-der

206 These results demonstrated that hepatic stellate cell-induced MDSCs concurrently suppress both T

207 Cells showed decreased fibrogenesis, hepatic stellate cell infiltration, Kupffer cells and inflammato

208 niaturized and integrated with human hepatic stellate cells inside microfluidic devices.

209 Furthermore, T-stellate cells integrate D-stellate inhibition from an a

210 We find that in cerebellar stellate cell interneurons of mice, the composition and

211 Furthermore, the IH current present in stellate cells is critical to the enhanced spike phase-l

212 responses by random voltage fluctuations in stellate cells is significantly limited.

213 pairment in inhibitory synaptic responses in stellate cells lacking NL123 despite a nearly complete s

214 olate induced cytosolic Ca(2+) elevations in stellate cells, larger than those elicited simultaneousl

215 activity and isoprenylation are required for stellate cell LD loss and induction of activation marker

216 idenced by chloride ion movement through the stellate cells, leading to depolarization of the transep

217 LE) on the activation of human liver hepatic stellate cell line LX-2 cells.

218 This mechanism was confirmed in a hepatic stellate cell line stably that endogenously expresses RX

219 ted PRHs was applied to cultured rat hepatic stellate cell line, HSC-T6, with or without Flu-pretreat

220 involving the TRAIL receptors in the hepatic stellate cell line, LX2.

221 ulation; coculture of hepatocyte and hepatic stellate cell lines significantly increased expression o

222 fibrogenic program in hepatocyte and hepatic stellate cell lines through ROS, NFkappaB, and TGFbeta1

223 of IKK2 (3 months) resulted in activation of stellate cells, loss of acinar cells, and fibrosis, whic

224 tumor stroma had fewer activated pancreatic stellate cells, lower levels of periostin, and alteratio

225 lloproteinase-1 secretion induced by hepatic stellate cells (LX-2).

226 med in vitro studies on immortalized hepatic stellate cells (LX-2).

227 ssor EID1 in hepatoma cells Huh7, Hepa1, and stellate cells LX2.

228 up to 21 days using human cell lines hepatic stellate cells (LX2), hepatocellular carcinoma (Sk-Hep-1

229 f hepatocyte markers, oval cell markers, and stellate cell markers.

230 ndence for the exponential term that matches stellate cell membrane properties, a low degree of fluct

231 ns observed with collagen matrices including stellate cell morphologies, cell-mediated realignment of

232 es employing Tg technology to target hepatic stellate cells, myofibroblasts, liver sinusoidal endothe

233 esponses in medial entorhinal cortical (MEC) stellate cells of rats, which express strong sub-thresho

234 , mutation or RNAi-mediated knockdown in the stellate cells of the tubule of TAR2 (tyrR, CG7431) resu

235 e dendritic spine Ca(2+) signals in L4 spiny stellate cells of the vibrissal mouse cortex in vivo.

236 to monitor TGF-beta1 release from activated stellate cells over the course of 20 h.

237 tate transaminase, alanine transaminase, and stellate cell proliferation by up to 50-100%.

238 f aberrant GluN2C-mediated currents in spiny stellate cells promotes excessive temporal integration o

239 Recent findings implicate pancreatic stellate cells (PSC) as prominent mediators of inflammat

240 ber 17 (SLC22A17) in human pancreatic cancer stellate cells (PSC), key mediators of the PDAC stroma.

241 ciated fibroblasts [also known as pancreatic stellate cells (PSC)] and immune cells that provide a fi

242 oplasia, which is orchestrated by pancreatic stellate cells (PSCs) and accounts for the majority of t

243 rix proteoglycan overexpressed by pancreatic stellate cells (PSCs) and pancreatic ductal adenocarcino

244 demonstrate that mouse and human pancreatic stellate cells (PSCs) are a source of IL-4/IL-13.

245 Pancreatic stellate cells (PSCs) are key mediators in the productio

246 Normal pancreatic stellate cells (PSCs) are regarded as quiescent, only to

247 Persistent activation of pancreatic stellate cells (PSCs) can perturb the biomechanical homo

248 Pancreatic stellate cells (PSCs) differentiate into cancer-associat

249 version of quiescent to activated pancreatic stellate cells (PSCs) drives the severe stromal reaction

250 activation of myofibroblast-like pancreatic stellate cells (PSCs) plays a predominant role in the fo

251 Conversely, TLR9 ligation induces pancreatic stellate cells (PSCs) to become fibrogenic and secrete c

252 er of myofibroblasts or activated pancreatic stellate cells (PSCs)).

253 nalling between pancreatic acinar (PACs) and stellate cells (PSCs).

254 a common phenomenon of activated pancreatic stellate cells (PSCs)/fibroblasts, the major stromal cel

255 or olive glycinergic synapse, and the basket/stellate cell-Purkinje GABAergic synapse in the cerebell

256 Contrary to the stellate cells, pyramidal cells show weaker temporal cod

257 ory projection cell classes, the bushy and T-stellate cells, receive a spatially broad inhibition fro

258 he ventral cochlear nucleus, the bushy and T-stellate cells, receive glycinergic inhibition with diff

259 A subset of both bushy and T-stellate cells receives inhibition from an unidentified

260 parate putative pyramidal cells and putative stellate cells recorded extracellularly in layer II of t

261 Overexpression of miR-29 in activated stellate cells reduced stromal deposition, cancer cell v

262 brosis, attenuated the activation of hepatic stellate cells, reduced frequencies of Th9, Th17 and Th1

263 ver, bile acid-elicited signalling events in stellate cells remain unexplored.

264 Transplanted stellate cells repopulated the damaged rat liver by cont

265 d -transporting hepatocytes, suggesting that stellate cells represent a source of liver progenitor ce

266 Yet by recording from axons of cerebellar stellate cell (SC) interneurons, we show that AP width v

267 ffer (KC), sinusoidal endothelial (LSEC) and stellate cells (SC) are major cellular components of the

268 Stellate cells (SCs) of MEC layer II provide major input

269 s (BCs) in the mouse cochlear nucleus with T-stellate cells (SCs), which do have normal overshooting

270 tigate Kv2 channel functions in mEC layer II stellate cells (SCs).

271 Primary hepatic stellate cell-seeded hydrogels stiffened in situ at late

272 ctin mRNA), whereas EX increased the hepatic stellate cell senescence marker CCN1 (P < 0.01 vs. O-SED

273 ell types show phase precession but putative stellate cells show steeper slopes of phase precession a

274 Stellate cell-specific expression of the teashirt paralo

275 lly contributed to climbing-fiber and basket/stellate-cell synapse functions, such that inhibitory sy

276 ffects of neuroligin deletions on cerebellar stellate cell synapses by electrophysiology in acute sli

277 t cell synapses, but not at distal dendritic stellate cell synapses.

278 gins increased the size of inhibitory basket/stellate-cell synapses but simultaneously severely impai

279 put image-based screen using primary hepatic stellate cells that identified the antifungal drug itrac

280 tion of GSG1L into mouse cultured cerebellar stellate cells that lack this protein increased the inwa

281 iber (PF) to PC synapses and DSI at putative Stellate cell to PC synapses.

282 ivation of the autophagic pathway in hepatic stellate cells to create a microenvironment that promote

283 AIL pathway can mediate apoptosis of hepatic stellate cells to promote the resolution of liver fibros

284 f CYLD, gene transcription of HGF in hepatic stellate cells was repressed through binding of histone

285 DNA damage, whereas proliferation of hepatic stellate cells was stimulated by KCa3.1 inhibition.

286 nces and synaptic input in medial entorhinal stellate cells, we performed patch-clamp recordings in m

287 Together with our recent findings on stellate cells, we propose a general mechanism by which

288 Primary pancreatic stellate cells were activated in vitro by C5a.

289 To further validate aptasensor responses, stellate cells were stained for markers of activation (e

290 howed that macrophages and activated hepatic stellate cells were the main cell types expressing PTX3

291 2 emerged around birth while reelin-positive stellate-cells were scattered throughout development.

292 CCN1 also induced Jag1 expression in hepatic stellate cells, whereupon they interacted with hepatic p

293 The inflammatory cells activate hepatic stellate cells, which are the major source of myofibrobl

294 hat the activation of perisinusoidal hepatic stellate cells, which is a key event mediating the augme

295 signaling may lead to activation of hepatic stellate cells, which is required for fibrosis.

296 change with the identification of pancreatic stellate cells, which produce the pancreatic tumor strom

297 d treatment caused necrosis predominantly in stellate cells, which was abolished by removal of extrac

298 Astrocytes are stellate cells whose appearance can resemble a pointed s

299 We previously demonstrated that pancreatic stellate cells within pancreatic ductal adenocarcinoma (

300 Mechanistically, PTX3 mediated the hepatic stellate cell wound-healing response.