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1 d in the liver, their expansion supported by hepatic stellate cells.
2 in embryonic stem cells, gastric tumors, and hepatic stellate cells.
3 ibrogenesis is limited compared with that of hepatic stellate cells.
4 GPR55 in mice, human hepatocytes, and human hepatic stellate cells.
5 l, the L4F nanoparticles were incubated with hepatic stellate cells.
6 pha SMA) revealed a significant reduction in hepatic stellate cells.
7 patocytes, sinusoidal endothelial cells, and hepatic stellate cells.
8 ctivation of neutrophils, Kupffer cells, and hepatic stellate cells.
9 secretion and inhibit collagen deposition in hepatic stellate cells.
10 ta (TGF-beta) signaling pathway in activated hepatic stellate cells.
11 mune response induced by B. abortus-infected hepatic stellate cells.
12 stern diet, indicating reduced activation of hepatic stellate cells.
13 both preneoplastic hepatocytes and activated hepatic stellate cells.
14 duces hepatocyte growth factor production by hepatic stellate cells.
15 les and vitamin A storage, resembled that of hepatic stellate cells.
16 sociated fibroblasts, dermal fibroblasts and hepatic stellate cells.
17 a1) expression suppresses MICA expression in hepatic stellate cells.
18 ocytes activates fibrosis-related markers in hepatic stellate cells.
19 C), as well as primary human hepatocytes and hepatic stellate cells.
20 fibrosis marker activation in primary human hepatic stellate cells.
21 e lineage tracing to follow transplanted rat hepatic stellate cells, a resident liver mesenchymal cel
22 lic fatty liver disease activity scores, and hepatic stellate cell activation (alpha-smooth muscle ac
23 th hepatic alphaSMA expression, a marker for hepatic stellate cell activation (r = -0.31, P < 0.02).
24 hat coincided with alterations in markers of hepatic stellate cell activation and extracellular matri
25 dently benefitted liver fibrosis via altered hepatic stellate cell activation and extracellular matri
28 evance, C1QTNF2 expression is reduced during hepatic stellate cell activation in culture and in a mou
33 idence demonstrate that the hepatic fibrosis/hepatic stellate cell activation may be an important gen
34 suppression of infiltrating macrophages and hepatic stellate cell activation through modulation of i
36 olic zonation, sinusoid capillarization, and hepatic stellate cell activation were assessed by anti-c
37 mes resulting in hyperammonemia, evidence of hepatic stellate cell activation, and progressive fibros
38 enesis partly mediated through inhibition of hepatic stellate cell activation, and significant decrea
39 ction induced liver fibrosis associated with hepatic stellate cell activation, hepatitis, and liver i
40 ary proliferation, senescence, fibrosis, and hepatic stellate cell activation, which were reduced in
48 tivated myofibroblastic phenotype (activated hepatic stellate cell; aHSCs) expressing smooth muscle a
53 ile a smaller fraction of NPs accumulated in hepatic stellate cells and liver sinusoidal endothelial
54 HCC cells under normoxia and hypoxia, human hepatic stellate cells and LX2 cells, and xenograft tumo
55 ein interactors for galectin-3 in live human hepatic stellate cells and peripheral blood mononuclear
56 triggering cellular senescence in activated hepatic stellate cells and portal fibroblasts by engagin
57 e system to study differentiation of primary hepatic stellate cells and portal fibroblasts from rats
58 ological events, including the activation of hepatic stellate cells and regulation of immune response
59 inct mesothelial cell types as well as early hepatic stellate cells and reveal distinct spatiotempora
61 he MIF receptor, CD74, that is released from hepatic stellate cells and that binds MIF, neutralizing
62 ells), LECs (Liver Endothelial Cells), HSCs (Hepatic Stellate Cells) and/or myofibroblasts to mimic i
63 rate fibrosis in a yin-yang interaction with hepatic stellate cells, and are a key component of tumor
65 promotes fibrogenic activation of attenuated hepatic stellate cells, and limits fibrosis reversal.
66 with eosinophils, neutrophils, macrophages, hepatic stellate cells, and lymphocytes all identified a
68 sion of a subset of TGF-beta target genes in hepatic stellate cells, and the cooperation between the
73 ding of the formation and characteristics of hepatic stellate cells, as well as their function in liv
74 nistic target of rapamycin, likely targeting hepatic stellate cells because differentiation and activ
75 poptosis in CAF and in myofibroblastic human hepatic stellate cells but lacked similar effects in qui
76 ver, the major cellular source of HGF is the hepatic stellate cell, but after liver injury, HGF expre
77 s was accompanied by increased activation of hepatic stellate cells, but hepatic mediators of inflamm
78 mide-induced fibrosis, which requires motile hepatic stellate cells, but not from bile duct ligation-
80 o, AGE exposure decreased Sirt1 and Timp3 in hepatic stellate cells by a NOX2-dependent pathway, and
81 tly induced production of collagen type I in hepatic stellate cells by activating the signal transduc
82 large numbers of hepatocytes, Kupffer cells, hepatic stellate cells, CD4-positive and CD8-positive ly
84 is, hepatic Rho-kinase activity (a marker of hepatic stellate cell contraction), and the endothelial
86 inhibition of miR-200b in cholangiocytes and hepatic stellate cells decreased the expression of miR-2
87 issue inflammation accompanied with elevated hepatic stellate cell-derived TnC and Toll-like receptor
89 nd activities of hepatocytes, Kupffer cells, hepatic stellate cells, endothelial cells, and circulati
96 n the transcriptome of rat PMFs, compared to hepatic stellate cell HSC-derived myofibroblasts in cult
97 ceptor (A2AR) activation is known to enhance hepatic stellate cell (HSC) activation and A2AR deficien
98 istration of obeticholic acid (OCA) prevents hepatic stellate cell (HSC) activation and fibrogenesis.
99 ing on the role of inflammatory mediators in hepatic stellate cell (HSC) activation and HSC survival
100 Liver X receptors (LXRs) are determinants of hepatic stellate cell (HSC) activation and liver fibrosi
101 such as dendritic cells (DCs) contribute to hepatic stellate cell (HSC) activation and liver fibrosi
102 ceptor tyrosine kinases, which contribute to hepatic stellate cell (HSC) activation and liver fibrosi
115 These pathways included overexpression of hepatic stellate cell (HSC) activators such as fibronect
116 M-CSF-Mphi and IL-34-Mphi also express the hepatic stellate cell (HSC) activators, platelet-derived
117 e role and the molecular mediators of EMT in hepatic stellate cell (HSC) and human liver cancer cells
118 study was to identify the role of Nogo-B in hepatic stellate cell (HSC) apoptosis in cirrhotic liver
121 tor type 4 (CXCR4) pathway directly promotes hepatic stellate cell (HSC) differentiation and activati
122 thymosin beta-4 (TB4) involved in regulating hepatic stellate cell (HSC) functions remain unclear.
123 MPI in zebrafish liver in vivo and in human hepatic stellate cell (HSC) lines in culture activates f
125 YK expression in the parenchymal hepatocyte, hepatic stellate cell (HSC), and the inflammatory compar
126 sition of extracellular matrix components by hepatic stellate cell (HSC)-derived myofibroblasts.
127 reaction (qRT-PCR) and western blotting and hepatic stellate cell (HSC)-MF contractility by gel cont
128 eceptor type 2 (CCR2) is expressed by active hepatic stellate cells (HSC) and is a key monocyte recru
129 larifying the crosstalk of hepatocytes (HC), hepatic stellate cells (HSC) and liver sinusoidal endoth
130 Erlotinib reduced EGFR phosphorylation in hepatic stellate cells (HSC) and reduced the total numbe
131 ion would normalize crosstalk with activated hepatic stellate cells (HSC) and thereby promote quiesce
137 n (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study.
139 s ectopically expressed during activation of hepatic stellate cells (HSC) when it is responsible for
140 -22 ameliorates liver fibrosis by inhibiting hepatic stellate cells (HSC), and loss of miR-200a is as
141 in response (UPR) both promote activation of hepatic stellate cells (HSC), however the link between t
142 e influence on viability and mitochondria of hepatic stellate cells (HSC), the toxicity of the codrug
145 system (MLH) comprising primary macrophages, hepatic stellate cells (HSC, LX-2), and hepatocytes (Huh
146 ole of secreted bioactive TGF-beta1 in human hepatic stellate cells (HSCs) activation and invasion.
147 on-kinse (FAK) plays a key role in promoting hepatic stellate cells (HSCs) activation in vitro and li
148 (CTGF) is constantly expressed in activated hepatic stellate cells (HSCs) and acts downstream of TGF
149 was principally expressed in quiescent mouse hepatic stellate cells (HSCs) and directly suppressed pr
150 OPN biological actions were studied in human hepatic stellate cells (HSCs) and in precision-cut liver
151 ed the anti-fibrotic effects of neratinib in hepatic stellate cells (HSCs) and in vivo models of CCl(
152 A to regulate transcription, is expressed by hepatic stellate cells (HSCs) and is required for develo
154 n induce liver fibrosis remission by killing hepatic stellate cells (HSCs) and producing interferon (
155 Liver repair involves phenotypic changes in hepatic stellate cells (HSCs) and reactivation of morpho
157 that accumulate during tissue fibrosis, and hepatic stellate cells (HSCs) are believed to be the maj
162 ha-actin (SM alpha-actin) is up-regulated in hepatic stellate cells (HSCs) as they transition to myof
163 e factor-1alpha (HIF-1alpha) is activated in hepatic stellate cells (HSCs) by hypoxia and regulates g
164 he hypothesis that the NLRP3 inflammasome in hepatic stellate cells (HSCs) can directly regulate thei
166 tyrosine kinase receptor, is up-regulated in hepatic stellate cells (HSCs) during chronic liver injur
171 t the potential role of progenitor cells and hepatic stellate cells (HSCs) in promoting the early eve
173 hepatic gammadelta T cells colocalized with hepatic stellate cells (HSCs) in vivo and promoted apopt
183 onic liver disease mediated by activation of hepatic stellate cells (HSCs) leads to liver fibrosis.
185 Proliferating cholangiocytes and activated hepatic stellate cells (HSCs) participate in the promoti
189 ammatory and pro-fibrogenic environment with hepatic stellate cells (HSCs) remodeling the extracellul
191 (NKT) cells to the liver to remove activated hepatic stellate cells (HSCs) significantly and ameliora
193 n of matrix proteins, such as collagen I, by hepatic stellate cells (HSCs) that culminates in cirrhos
194 developed a novel model for depleting mouse hepatic stellate cells (HSCs) that has allowed us to cla
201 novel Cre-transgenic mouse that marks 99% of hepatic stellate cells (HSCs), a liver-specific pericyte
203 ading to increased LPA levels, activation of hepatic stellate cells (HSCs), and amplification of prof
205 o-fibrogenic microenvironment, activation of hepatic stellate cells (HSCs), and progression of biliar
206 ver sinusoidal endothelial cells (LSECs) and hepatic stellate cells (HSCs), are the first liver cells
207 ion of myofibroblasts derived from quiescent hepatic stellate cells (HSCs), but the mechanisms that c
208 tion of liver disease is mostly displayed in hepatic stellate cells (HSCs), causing fibrosis/cirrhosi
209 acellular matrix (ECM) cytokine expressed in hepatic stellate cells (HSCs), could drive fibrogenesis
211 lls of the gastrointestinal tract, including hepatic stellate cells (HSCs), endothelial cells, and he
212 oncomitant with activation and senescence of hepatic stellate cells (HSCs), exhibiting a senescence-a
213 of nonalcoholic steatohepatitis (NASH) using hepatic stellate cells (HSCs), hepatocytes, and mouse mo
214 periments were performed with primary rodent hepatic stellate cells (HSCs), Kupffer cells (KCs), and
216 78a-3p, directly targeting Gli3 in activated hepatic stellate cells (HSCs), reduces expression of Gli
217 yte-macrophage colony-stimulating factor and hepatic stellate cells (HSCs), resulting in the generati
218 tamoxifen promotes mechanical quiescence in hepatic stellate cells (HSCs), stromal fibroblast-like c
220 levels of IL-10R2 and IL-22R1 expression on hepatic stellate cells (HSCs), the predominant cell type
223 at TGF-beta1 recruited IQGAP1 to TbetaRII in hepatic stellate cells (HSCs), the resident liver pericy
224 uct ligation (BDL) and in cultured activated hepatic stellate cells (HSCs), we show that OPN, besides
225 mechanism of this resistance by focusing on hepatic stellate cells (HSCs), which are known to regula
227 wth factor beta (TGFbeta) potently activates hepatic stellate cells (HSCs), which promotes production
245 of IL-20 was much higher in hepatocytes and hepatic stellate cells in liver biopsies from patients w
246 ivated B cells (NFkappaB) in hepatocytes and hepatic stellate cells in monoculture; however, they do
248 inhibition of miR-200b in cholangiocytes and hepatic stellate cells in vitro, we evaluated angiogenes
249 ion of a p53-dependent senescence program in hepatic stellate cells increases liver fibrosis and cirr
250 on of tumor-derived JAG1 signaling activated hepatic stellate cells, increasing their recruitment to
254 r was miniaturized and integrated with human hepatic stellate cells inside microfluidic devices.
256 ing LHX2, but not in co-culture with a human hepatic stellate cell line (LX-2) overexpressing LHX2.
259 PA-treated PRHs was applied to cultured rat hepatic stellate cell line, HSC-T6, with or without Flu-
261 1 up-regulation; coculture of hepatocyte and hepatic stellate cell lines significantly increased expr
262 iven profibrogenic program in hepatocyte and hepatic stellate cell lines through ROS, NFkappaB, and T
267 ted for up to 21 days using human cell lines hepatic stellate cells (LX2), hepatocellular carcinoma (
268 to activate cultured fibroblasts and primary hepatic stellate cells (myofibroblast precursors in the
269 of studies employing Tg technology to target hepatic stellate cells, myofibroblasts, liver sinusoidal
270 ed production of hepatocyte growth factor in hepatic stellate cells postinjury, which, in turn, resul
272 patic fibrosis, attenuated the activation of hepatic stellate cells, reduced frequencies of Th9, Th17
273 ors, liver sinusoidal endothelial cells, and hepatic stellate cells respond to liver injury and contr
275 muscle actin mRNA), whereas EX increased the hepatic stellate cell senescence marker CCN1 (P < 0.01 v
277 throughput image-based screen using primary hepatic stellate cells that identified the antifungal dr
278 9 (BMP9) is a circulating factor produced by hepatic stellate cells that plays a critical role in vas
279 as major active component) directly activate hepatic stellate cells, the fibrogenic cell in the liver
280 egression and reduced clearance of activated hepatic stellate cells, the key fibrogenic cell in the l
281 the activation of the autophagic pathway in hepatic stellate cells to create a microenvironment that
282 findings linking senescence and autophagy in hepatic stellate cells to HCC have also been discovered,
284 lls, liver sinusoidal endothelial cells, and hepatic stellate cells to liver homeostasis and repair a
285 The TRAIL pathway can mediate apoptosis of hepatic stellate cells to promote the resolution of live
286 bsence of CYLD, gene transcription of HGF in hepatic stellate cells was repressed through binding of
287 sis and DNA damage, whereas proliferation of hepatic stellate cells was stimulated by KCa3.1 inhibiti
288 nthesis; and as ammonia is known to activate hepatic stellate cells, we hypothesized that ammonia may
290 nation showed that macrophages and activated hepatic stellate cells were the main cell types expressi
293 parent that the activation of perisinusoidal hepatic stellate cells, which is a key event mediating t
294 sis of liver fibrosis involves activation of hepatic stellate cells, which is associated with depleti
295 -catenin signaling may lead to activation of hepatic stellate cells, which is required for fibrosis.
296 r disease can induce prolonged activation of hepatic stellate cells, which may result in liver fibros
297 omoting ADAM17-mediated shedding of TNFRs in hepatic stellate cells, which reduces TNFR signaling and
299 ons in vitro, we treated rat hepatocytes and hepatic stellate cells with PLS, which caused proteolyti