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1 1 in NL-fibroblasts increased collagen-I and alpha-smooth muscle actin.
2 oduction of extracellular matrix proteins or alpha-smooth muscle actin.
3 lphav, beta3, beta1, alpha2(I) collagen, and alpha-smooth muscle actin.
4 in and acquisition of the mesenchymal marker alpha-smooth muscle actin.
5 nail, Slug/Snai2, vimentin, fibronectin, and alpha-smooth muscle actin.
6 markers, including collagen IV, laminin, and alpha-smooth muscle actin.
7 lso formed vascular structures and expressed alpha-smooth muscle actin.
8 nduce expression of the myofibroblast marker alpha-smooth muscle actin.
9 induced a fibroblast phenotype negative for alpha-smooth muscle actin.
10 ificant increase in the myofibroblast marker alpha-smooth muscle actin.
11 beta, but not the smooth muscle cell marker alpha-smooth muscle actin.
12 onidazole, EF5, the Hoechst 33342, CD31, and alpha-smooth muscle actin.
13 of multilayered SMCs expressing calponin and alpha-smooth muscle actin.
14 onectin as well as the myofibroblast marker, alpha-smooth muscle actin.
15 receptor tyrosine kinase 2, fibronectin, and alpha-smooth muscle actin.
16 ated positively with that of fibronectin and alpha-smooth muscle actin.
17 infusion also reduced hepatic expression of alpha-smooth muscle actin (0.19 +/- 0.007-fold compared
18 y indicator, calponin loss intermediate, and alpha-smooth muscle actin a later indicator of compromis
19 y cancer cells expressed increased levels of alpha-smooth muscle actin, a marker of CAF, compared wit
21 nsitometry analyses showed less staining for alpha-smooth muscle actin, a myofibroblast marker, in th
22 east 4 genes: myosin heavy chain 11 (MYH11), alpha-smooth muscle actin (ACTA2), and transforming grow
24 1, only submesothelial fibroblasts expressed alpha-smooth muscle actin after induction of peritoneal
25 ne in TACE activity, procollagen alpha1 (I), alpha smooth muscle actin (alpha-SMA) and transforming g
26 e TGF-beta1 is critical for the induction of alpha smooth muscle actin (alpha-SMA) and type 1 collage
28 n of both CLIC4 and the myofibroblast marker alpha smooth muscle actin (alpha-SMA) in stromal fibrobl
29 utroban reduced liver fibrosis and decreased alpha smooth muscle actin (alpha-SMA), collagen-I, and t
30 Molecular assays revealed higher level of alpha smooth muscle actin (alpha-SMA), desmin, calponin,
35 ifferentiation and fibrotic markers, such as alpha-smooth muscle actin (alpha-SMA) and Collagen III (
36 n is associated with increased expression of alpha-smooth muscle actin (alpha-SMA) and collagen in fi
37 ary fibrosis and inhibits TGF-beta1-mediated alpha-smooth muscle actin (alpha-SMA) and collagen induc
38 n and an increase in the profibrotic markers alpha-smooth muscle actin (alpha-SMA) and fibronectin, a
39 tolic blood pressure and renal expression of alpha-smooth muscle actin (alpha-SMA) and proliferating
41 breast tumor models, Cellax therapy reduced alpha-smooth muscle actin (alpha-SMA) content by 82% and
42 ncluding an approximately 2-fold increase in alpha-smooth muscle actin (alpha-SMA) expression and str
43 E2 on proliferation, collagen secretion, and alpha-smooth muscle actin (alpha-SMA) expression was ass
44 inhibited the induction of activation marker alpha-smooth muscle actin (alpha-SMA) in rat and mouse H
46 Transcription of the contractile protein alpha-smooth muscle actin (alpha-SMA) is mediated by the
47 n content, and numbers of cells positive for alpha-smooth muscle actin (alpha-SMA) or phospho-Smad2 w
48 TP stimulation of P2Y(2) receptors increased alpha-smooth muscle actin (alpha-SMA) production, and in
49 ollagen deposition and reduced expression of alpha-smooth muscle actin (alpha-SMA) protein indicated
50 HIF-1alpha) activation of the TGF-beta/Smad3/alpha-smooth muscle actin (alpha-SMA) signaling pathway,
52 TCP and were analyzed for the expression of alpha-smooth muscle actin (alpha-SMA), a key marker of m
53 ation, cell proliferation, and expression of alpha-smooth muscle actin (alpha-SMA), a marker of PSC a
54 ch assay cell migration, immunocytochemistry alpha-smooth muscle actin (alpha-SMA), and collagen gel
55 ically confirmed via expression of vimentin, alpha-smooth muscle actin (alpha-SMA), and glial fibrill
56 ssions of NADPH oxidase gp91 (phox) subunit, alpha-smooth muscle actin (alpha-SMA), and NFkappaB p65
57 he three major myofibroblast markers, SDF-1, alpha-smooth muscle actin (alpha-SMA), and TGF-beta1, an
58 neal fibroblasts to up-regulate synthesis of alpha-smooth muscle actin (alpha-SMA), collagen 1 (COL1)
60 tion and activation, including expression of alpha-smooth muscle actin (alpha-SMA), collagen, and adh
61 metalloproteinase 2 (Mmp2), cytokeratin 19, alpha-smooth muscle actin (alpha-SMA), cytochrome P450 7
62 inant Shh protein activated Gli1 and induced alpha-smooth muscle actin (alpha-SMA), desmin, fibronect
63 he enhanced expression of fibrogenic markers alpha-smooth muscle actin (alpha-SMA), TGF-beta, and pro
64 cal examination as well as the expression of alpha-smooth muscle actin (alpha-SMA), transforming grow
66 n of EndoMT was assessed by determination of alpha-smooth muscle actin (alpha-SMA), type I collagen,
67 10 nM) did not modify the gene expression of alpha-smooth muscle actin (alpha-SMA), Vimentin (VIM), F
68 CCA has been associated with the presence of alpha-smooth muscle actin (alpha-SMA)-positive myofibrob
69 en deposition, immune cell infiltration, and alpha-smooth muscle actin (alpha-SMA)-positive myofibrob
70 duction of EMT resulted in the generation of alpha-smooth muscle actin (alpha-SMA)-positive myofibrob
71 -triggered differentiation into contractile, alpha-smooth muscle actin (alpha-SMA)-positive myofibrob
75 c NK cells were enriched in proximity to the alpha-smooth muscle actin (alpha-SMA+) area within mild
76 h signaling), sox-9 (progenitor marker), and alpha-smooth muscle actin (alpha-SMA; myofibroblast mark
77 rylated AKT [p-AKT](+)), and differentiated (alpha-smooth muscle actin [alpha-SMA](+)) fibrocytes wer
78 r with PDZ-binding motif, YAP/TAZ) and late (alpha-smooth muscle actin, alpha-SMA) markers of myofibr
79 MAP kinase, a substrate of MKP-1, as well as alpha smooth muscle actin (alphaSMA) expression in vesse
80 on, apoptosis, and number of (proliferating) alpha smooth muscle actin (alphaSMA) neointimal cells.
81 directly binds to the regulatory regions of alpha smooth muscle actin (alphaSMA), collagen I, tissue
84 hymal transition (EMT) and the expression of alpha-smooth muscle actin (alphaSMA) and matrix metallop
85 es and analyzed for the myofibroblast marker alpha-smooth muscle actin (alphaSMA) and Smad7 expressio
86 roliferating cell nuclear antigen (PCNA) and alpha-smooth muscle actin (alphaSMA) double-immunostaini
87 tivated primary HSCs, confirmed by increased alpha-smooth muscle actin (alphaSMA) expression and enha
88 4 on HLMF proliferation, collagen secretion, alpha-smooth muscle actin (alphaSMA) expression, and Sma
90 AF subpopulation with elevated expression of alpha-smooth muscle actin (alphaSMA) located immediately
94 h stereomicroscopy, slit lamp biomicroscopy, alpha-smooth muscle actin (alphaSMA), fibronectin, and F
97 xpressed in mesenchymal cells that expressed alpha-smooth muscle actin and activated BMP signaling pa
98 ens of macular pseudoholes were positive for alpha-smooth muscle actin and anti-glial fibrillary acid
100 f smooth muscle cell differentiation markers alpha-smooth muscle actin and calponin implicating its i
102 and reduced expression of TGF-beta1-induced alpha-smooth muscle actin and collagen alpha-2(I) but no
104 pha increased the survival of HSCs and their alpha-smooth muscle actin and collagen I expression, thu
106 cription factor-1 and the mesenchymal marker alpha-smooth muscle actin and CXCR3 expression was exami
107 iation is characterized by the expression of alpha-smooth muscle actin and extracellular matrix prote
108 rin, and the increase in mesenchymal markers alpha-smooth muscle actin and fibroblast-specific protei
109 ctivated freshly isolated HSCs (induction of alpha-smooth muscle actin and fibrosis-associated genes)
110 ce treated with RF ablation were stained for alpha-smooth muscle actin and Ki-67 to establish the rol
111 cell proliferation, including expression of alpha-smooth muscle actin and matrix accumulation of fib
112 Rivaroxaban deactivated HSC, with decreased alpha-smooth muscle actin and mRNA expression of other H
113 e EMyT manifested by increased expression of alpha-smooth muscle actin and other contractile proteins
114 , vimentin, the matrix metalloprotease MMP2, alpha-smooth muscle actin and phospho-Smad2, as well as
116 otoxicity showed significantly greater Nox2, alpha-smooth muscle actin and picrosirius levels compare
117 c-5 expression was associated with increased alpha-smooth muscle actin and plasminogen activator inhi
119 llagen type I mRNAs, large fibrotic areas in alpha-smooth muscle actin and Sirius red staining, and i
121 accompanied subsequently with stimulation of alpha-smooth muscle actin and type I collagen expression
122 ter numbers of myofibroblasts that expressed alpha-smooth muscle actin and vimentin than controls.
123 beta, beta-catenin, and mesenchymal markers (alpha-smooth muscle actin and vimentin) at both the gene
124 ere stained for markers of activation (e.g., alpha smooth muscle actin) and were also tested for pres
125 ducing levels of a marker of HSC activation (alpha-smooth muscle actin) and expression of genes that
126 phorylation), myofibroblast differentiation (alpha-smooth muscle actin), and collagen deposition (Mas
127 ctor alpha, transforming growth factor beta, alpha smooth muscle actin, and collagen (P < 0.01).
129 hymal markers, including collagen type I and alpha-smooth muscle actin, and a reduction in endothelia
130 nd immunohistochemistry for CD29/CD45, CD146/alpha-smooth muscle actin, and c-kit demonstrated that t
132 r alpha, monocyte chemoattractant protein-1, alpha-smooth muscle actin, and collagen I and TIMP1 expr
133 r this purpose, quantification of TGF-beta1, alpha-smooth muscle actin, and collagen type I mRNA and
135 of less organized intimal collagen, laminin, alpha-smooth muscle actin, and matrix-rich fibrosis was
136 tren's patients, reduced their expression of alpha-smooth muscle actin, and mediated disassembly of t
137 ignificantly less expression of collagen IV, alpha-smooth muscle actin, and other markers of disease
138 , collagen (Col) alpha1(I), Col alpha1(III), alpha-smooth muscle actin, and p-Smad2/3 was characteriz
140 -catenin and attenuated lung Snail1, Twist1, alpha-smooth muscle actin, and type I collagen accumulat
141 Snai1, and Snai2; by immunofluorescence for alpha-smooth muscle actin; and by Western blot analysis
142 ssed Snai1 and vimentin alongside nestin and alpha smooth muscle actin (another biomarker of EMT).
143 ted pericytes characterized by expression of alpha-smooth muscle actin are located adjacent to the te
144 geny of individual VSMCs contributes to both alpha smooth muscle actin (aSma)-positive fibrous cap an
145 in the expression of HSC-activation markers (alpha smooth muscle actin, beta platelet-derived growth
146 gen I gene expression by 64% (P = 0.001) and alpha-smooth muscle actin by 43% (P = 0.005) compared to
147 d with mesenchymal smooth muscle epitopes of alpha-smooth muscle actin, caldesmon and calponin, which
148 ssion of the cardinal myofibroblast products alpha smooth muscle actin, calponin, and collagen in pri
149 by nuclear magnetic resonance spectroscopy; alpha-smooth muscle actin, calponin, and LDH5 expression
150 n mothers against decapentaplegic homolog 4, alpha-smooth muscle actin, CD31, phospho-vascular endoth
151 howed normal outgrowth of mouse ERG-positive/alpha-smooth muscle actin coimmunolocalized cells; howev
152 ssical fibrocytes, they display cell surface alpha smooth muscle actin, collagen I/V, and mediate ang
153 lpha, led to a significant downregulation of alpha-smooth muscle actin, collagen I and III and decrea
154 TGF-beta as confirmed by strong induction of alpha-smooth muscle actin, collagen type I (COL1A1), and
155 e fibroblast proliferation and expression of alpha-smooth muscle actin, collagen, and other extracell
156 he expression of the fibrosis-related genes, alpha-smooth muscle actin, collagen-1, and collagen-3; r
157 F-actin, phosphorylated myosin light chain, alpha-smooth muscle actin, collagen-1A, and total collag
158 cores, and hepatic stellate cell activation (alpha-smooth muscle actin) compared to Long-Evans Tokush
159 sed expression of fibronectin-1, collagen I, alpha-smooth muscle actin, connective tissue growth fact
160 fibrotic components, including fibronectin, alpha-smooth muscle actin, connective tissue growth fact
161 ammatory cell infiltration, and collagen and alpha-smooth muscle actin content in their kidneys.
162 ression levels of fibronectin-1, collagen I, alpha-smooth muscle actin, CTGF, and PAI-1, but decrease
164 teoblasts, endothelial cells, Schwann cells, alpha-smooth muscle actin-expressing macrophages and mes
165 ) involves predominantly the accumulation of alpha-smooth muscle actin-expressing mesenchymal-like ce
166 fibrosis (IPF) involves the accumulation of alpha-smooth muscle actin-expressing myofibroblasts aris
167 serve as a receptor for the HU177 epitope in alpha-smooth muscle actin-expressing stromal cells and s
168 nesis and, surprisingly, the accumulation of alpha-smooth muscle actin-expressing stromal cells.
169 on to a mesenchymal phenotype with increased alpha smooth muscle actin expression and suppression of
170 s, coupled to a reduction in fibronectin and alpha smooth muscle actin expression in stromal fibrobla
172 tion together with increased fibronectin and alpha-smooth muscle actin expression and decreased in E-
173 cation of troglitazone significantly reduced alpha-smooth muscle actin expression and haze in the str
175 ice led to more abundant vascular and airway alpha-smooth muscle actin expression and inflammatory pu
177 d both MMP-9-induced TGF-beta activation and alpha-smooth muscle actin expression by displacing MMP-9
179 M(-/-), mice promoted increased collagen and alpha-smooth muscle actin expression from lung fibroblas
180 gest that both pro- and active MMP-9 trigger alpha-smooth muscle actin expression in cultured fibrobl
181 ta-galactosidase-positive HSCs and decreased alpha-smooth muscle actin expression in fibrotic livers
184 nectin, transforming growth factor-beta, and alpha-smooth muscle actin expression in obstructed kidne
186 knockdown of Has2 in SF, significantly less alpha-smooth muscle actin expression was detected in co-
188 terstitial fibrosis, a fivefold reduction in alpha-smooth muscle actin expression, and a 2.4-fold red
189 broblasts from AF dogs, proliferation rates, alpha-smooth muscle actin expression, and extracellular
190 oblasts populating collagen pads, attenuated alpha-smooth muscle actin expression, and stimulated mat
191 ted with fibronectin deposition, increase in alpha-smooth muscle actin expression, and the release of
192 on and genetic silencing of Cat B diminished alpha-smooth muscle actin expression, delayed fibroblast
193 d Akt signaling axis, increased collagen and alpha-smooth muscle actin expression, distinct gene expr
194 ured epithelial cells promote proliferation, alpha-smooth muscle actin expression, F-actin expression
195 s lacking endogenous sFRP-1 showed increased alpha-smooth muscle actin expression, higher cell prolif
196 onists tested in diverse cell models blocked alpha-smooth muscle actin expression, myofibroblast diff
199 ological changes including the expression of alpha-smooth muscle actin, fibronectin and TGFbeta-1 com
200 y quantitative polymerase chain reaction for alpha-smooth muscle actin, fibronectin, collagen type 1a
201 connective tissue growth factor (CTGF), and alpha-smooth muscle actin gene expression at 7 days, com
204 re than 30 mutations in ACTA2, which encodes alpha-smooth muscle actin, have been identified to cause
205 o missense mutations in ACTA2, which encodes alpha-smooth muscle actin, have been identified to cause
206 for hematoxylin and eosin, Masson trichrome, alpha-smooth muscle actin, IL-33, CD8, and IL-13 and ana
207 /7 receptor inhibitors blocked expression of alpha-smooth muscle actin in ASC in the absence of direc
208 ardiomyogenic markers cardiac troponin T and alpha-smooth muscle actin in CPCedeltaB compared with CP
209 was notably upregulated along with Col-1 and alpha-smooth muscle actin in pleural thickening in the c
212 pressions of two EMT markers (E-cadherin and alpha-smooth muscle actin) in the hGE cells after CsA tr
214 e arrest, and strongly reduced expression of alpha smooth muscle actin, indicating deficient HSC acti
215 dulin increased expression of collagen I and alpha-smooth muscle actin, indicating increased activati
218 (transforming growth factor-beta protein and alpha-smooth muscle actin mRNA), whereas EX increased th
220 nd tissue inhibitor metalloproteinase-1, and alpha-smooth muscle actin (myofibroblasts) were evaluate
221 xpression of selective VSMCs markers such as alpha smooth muscle actin, myosin heavy chain 11, and sm
222 d effectors, including collagens I and V and alpha-smooth muscle actin, on the transcript and protein
224 Green fluorescent protein costaining with alpha-smooth muscle actin or collagen 1alpha in left ven
225 of the adenoma stroma; cells that expressed alpha-smooth muscle actin or desmin were lost, along wit
226 ith bean-shaped condensed nuclei, absence of alpha-smooth muscle actin or stress fibres, and a corres
227 ed miR-199a-5p-dependent inhibition of CCN2, alpha-smooth muscle actin, or collagen 1(alpha1) in acti
229 model), hepatocyte growth factor (P<0.0001), alpha-smooth muscle actin (P<0.0001), fibronectin 1 (P<0
230 nd the amniotic membrane at 6 hours, whereas alpha-smooth muscle actin, phosphorylated Smad3, and col
231 peroxide, hydroxynonenal), and fibrogenesis (alpha-smooth muscle actin, picrosirius red, trichrome, v
232 d ATP but also increased basal expression of alpha-smooth muscle actin, plasminogen activator inhibit
233 timulation resulted in stably differentiated alpha-smooth muscle actin(+)/platelet-derived growth fac
234 ced fibrogenic activity (e.g., expression of alpha smooth muscle actin, platelet-derived growth facto
236 eveloped severe TV with intimal hyperplasia (alpha-smooth muscle actin positive cells in the neointim
238 t inhibition reduced fibrosis as measured by alpha-smooth muscle actin positive myofibroblasts and co
239 ne of the coagulation zone was surrounded by alpha-smooth muscle actin-positive activated myofibrobla
240 ng growth factors and cytokines, decrease of alpha-smooth muscle actin-positive ASFs, and finally in
241 th factor receptor-alpha-positive cells, and alpha-smooth muscle actin-positive blood vessels were as
242 wth factor receptor-alpha-positive cells, 4) alpha-smooth muscle actin-positive blood vessels, and 5)
243 erized by increased macrophage and decreased alpha-smooth muscle actin-positive cell population, fibr
245 a isoform co-localized with CD31-positive or alpha-smooth muscle actin-positive cells at different de
246 Cs and a 1.35-fold increase in proliferative alpha-smooth muscle actin-positive cells in the lungs of
247 bitor-1, and with a significant reduction in alpha-smooth muscle actin-positive cells in the renal in
248 ll thickening, and abnormal proliferation of alpha-smooth muscle actin-positive cells, as well as inc
249 dentified the presence von Willebrand factor/alpha-smooth muscle actin-positive endothelial cells in
250 elial-to-mesenchymal transition, detected as alpha-smooth muscle actin-positive endothelial cells, si
251 rthermore, treatment with cysteamine reduced alpha-smooth muscle actin-positive interstitial myofibro
252 lial fibroblasts are specific progenitors of alpha-smooth muscle actin-positive myofibroblasts that a
253 e relative abundance of both macrophages and alpha-smooth muscle actin-positive myofibroblasts was re
256 ated marked increases in calponin levels and alpha-smooth muscle actin-positive SMC areas in their at
258 vated fibroblasts, shown by up-regulation of alpha-smooth muscle actin, pro-collagen 1, and F-actin e
259 II-induced Ca(2+) influx, proliferation, and alpha-smooth muscle actin protein expression in fibrobla
260 ss cytotoxic, and a more potent inhibitor of alpha-smooth muscle actin protein expression than CCG-20
261 tenuated fibrotic markers such as diminished alpha-smooth muscle actin, reduced collagen deposition.
262 ASC migration toward EC and upregulation of alpha-smooth muscle actin, SM22alpha, and calponin expre
263 Although some TECs strikingly upregulate alpha smooth muscle actin (SMA), a principal marker of E
264 es, adiponectin stimulated the expression of alpha-smooth muscle actin (SMA) and extracellular matrix
266 s were tested for cell viability, apoptosis, alpha-smooth muscle actin (SMA), fibronectin (FN) produc
267 helial-mesenchymal transition (EMT) markers, alpha-smooth muscle actin (SMA), vimentin, and tenascin-
268 odies against selected stem cell markers and alpha-smooth muscle actin (SMA), which marks myoepitheli
269 on and remodeling of extracellular matrix by alpha-smooth muscle actin (SMA)-expressing myofibroblast
270 enal tubular epithelial cells transform into alpha-smooth muscle actin (SMA)-expressing myofibroblast
272 scle actin; and by Western blot analysis for alpha-smooth muscle actin, SNAIL1, SNAIL2, and the alpha
273 growth factor receptor-alpha, vimentin, and alpha-smooth muscle actin, specifying myofibroblasts as
275 of fibrosis-related genes, smaller areas of alpha-smooth muscle actin staining, and low collagen pro
277 and expression of collagen, fibronectin, and alpha-smooth muscle actin (substantially more than rapam
279 g; ii) factors controlling the expression of alpha-smooth muscle actin, the most used marker of myofi
280 ncreased both mRNA and protein expression of alpha-smooth muscle actin, transgelin, and calponin vers
281 roblast differentiation and up-regulation of alpha-smooth muscle actin, type I collagen, and fibronec
282 or submesothelial fibroblasts each expressed alpha-smooth muscle actin under the influence of TGF-bet
283 oblast differentiation (ED-A fibronectin and alpha-Smooth Muscle Actin) upon treatment with TGF-beta1
285 erin, and Integrins), cytoskeletal proteins (alpha-Smooth Muscle Actin, Vimentin, and beta-catenin),
287 corporation of EdU and protein expression of alpha-smooth muscle actin was analyzed by immunocytochem
289 sessed by Sirius red staining; expression of alpha-smooth muscle actin was measured by immunoblot ana
290 l differentiation markers p63, calponin, and alpha-smooth muscle actin was observed in the mouse myoe
292 notype, which is characterized by expressing alpha-smooth muscle actin, was inhibited and reverted by
294 and zona occludens-1, whereas collagen-I and alpha-smooth muscle actin were increased in ATII cells i
296 en 1, transforming growth factor beta-1, and alpha-smooth muscle actin were reduced, whereas tenascin
298 s against von Willebrand factor, VCAM-1, and alpha-smooth muscle actin, were measured for total area
299 , corneal fibrosis markers, Collagen III and alpha-smooth muscle actin, were significantly downregula
300 addition, we observed a significant loss of alpha-smooth muscle actin, which indicates a difference
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