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1 gy-dynamic but not fully differentiated from smooth muscle.
2 of individual elastic lamellae and vascular smooth muscle.
3 erties and the resting membrane potential of smooth muscle.
4 on bradykinin-induced contraction, in airway smooth muscle.
5 iveness: the excessive contraction of airway smooth muscle.
6 c field stimulation (EFS) in bovine tracheal smooth muscle.
7 ation of RLC phosphorylation in tonic airway smooth muscle.
8 apidity of pCPI-17 inactivation in mammalian smooth muscles.
9 f striated muscles and attachment plaques of smooth muscles.
11 ion also reduced hepatic expression of alpha-smooth muscle actin (0.19 +/- 0.007-fold compared with c
14 ssociated with increased expression of alpha-smooth muscle actin (alpha-SMA) and collagen in fibrotic
15 ted the induction of activation marker alpha-smooth muscle actin (alpha-SMA) in rat and mouse HSCs.
17 n of EMT resulted in the generation of alpha-smooth muscle actin (alpha-SMA)-positive myofibroblasts
18 osition, immune cell infiltration, and alpha-smooth muscle actin (alpha-SMA)-positive myofibroblasts.
19 ells were enriched in proximity to the alpha-smooth muscle actin (alpha-SMA+) area within mild fibros
20 population with elevated expression of alpha-smooth muscle actin (alphaSMA) located immediately adjac
23 nd the increase in mesenchymal markers alpha-smooth muscle actin and fibroblast-specific protein 1.
24 oxaban deactivated HSC, with decreased alpha-smooth muscle actin and mRNA expression of other HSC act
28 en fluorescent protein costaining with alpha-smooth muscle actin or collagen 1alpha in left ventricul
29 otoxic, and a more potent inhibitor of alpha-smooth muscle actin protein expression than CCG-203971.
32 er cells expressed increased levels of alpha-smooth muscle actin, a marker of CAF, compared with MSC
33 c flow contained reduced myosin heavy chain, smooth muscle actin, and desmin, and increased markers o
34 ted positively with CSE, myosin heavy chain, smooth muscle actin, and desmin, and negatively with cel
37 ers against decapentaplegic homolog 4, alpha-smooth muscle actin, CD31, phospho-vascular endothelial
38 pression of fibronectin-1, collagen I, alpha-smooth muscle actin, connective tissue growth factor (CT
39 n levels of fibronectin-1, collagen I, alpha-smooth muscle actin, CTGF, and PAI-1, but decreased Smad
40 ion of selective VSMCs markers such as alpha smooth muscle actin, myosin heavy chain 11, and smooth m
41 fibroblasts, shown by up-regulation of alpha-smooth muscle actin, pro-collagen 1, and F-actin express
42 sis (IPF) involves the accumulation of alpha-smooth muscle actin-expressing myofibroblasts arising fr
43 wth factors and cytokines, decrease of alpha-smooth muscle actin-positive ASFs, and finally in a sign
44 tor receptor-alpha-positive cells, and alpha-smooth muscle actin-positive blood vessels were assayed
45 ctor receptor-alpha-positive cells, 4) alpha-smooth muscle actin-positive blood vessels, and 5) of ke
46 a 1.35-fold increase in proliferative alpha-smooth muscle actin-positive cells in the lungs of ITSN-
51 l effects of infarct scar maturation, causes smooth muscle alpha-actin fiber formation, up-regulation
52 These findings reveal that disruption of smooth muscle alpha-actin filaments in smooth muscle cel
54 LAM is characterized by neoplastic growth of smooth muscle-alpha-actin-positive cells that destroy lu
56 ed blood vessels of all caliber and putative smooth muscle and astroglial basement membrane compartme
58 mote migration and proliferation of vascular smooth muscle and endothelial cells via P1 and P2Y recep
62 reases STOC activity in contractile vascular smooth muscle and show that a critical step is the activ
64 d epithelioid cells (LAM cells) that express smooth-muscle and melanocyte-lineage markers, harbor mTO
67 eosinophils, lung Il13 levels, collagen, and smooth muscle, as well as a significant depletion of gob
68 stent airflow obstruction had greater airway smooth muscle (Asm) area with decreased periostin and tr
69 mechanism along the cholinergic nerve-airway smooth muscle (ASM) axis that underlies prolonged airway
72 f human LTCCs during SN DA-like and arterial smooth muscle (aSM)-like activity patterns using whole-c
76 characterized by excessive pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and
78 ng to thoracic aortic disease either disrupt smooth muscle cell (SMC) contraction or adherence to an
82 sions of hyperglycemic ApoE(-/-) mice; also, smooth muscle cell (SMC), macrophage and leukocyte abund
83 elial cell (BmxCreER(T2)-driven)-specific or smooth muscle cell (SMC, SmmhcCreER(T2)- or TaglnCre-dri
85 in pathophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and proliferation.
86 articles were safe to rat pulmonary arterial smooth muscle cell and to the lungs, as evidenced by the
88 kinase inhibition directly attenuates airway smooth muscle cell contraction independent of its protec
91 (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315).
92 GAS5) suppresses TGF-beta/Smad3 signaling in smooth muscle cell differentiation of mesenchymal progen
93 wered blood pressure, which was dependent on smooth muscle cell expression of Panx1 and independent o
95 ar cell functions, including endothelial and smooth muscle cell growth, proliferation, and migration;
98 and evidence of higher biological activity (smooth muscle cell loss and fibrin deposition) in the FP
99 s levels substantially attenuated BI-induced smooth muscle cell migration and proliferation, resultin
100 llular phenotypes was analyzed with vascular smooth muscle cell migration assays and platelet aggrega
101 developed less neointimal hyperplasia, less smooth muscle cell proliferation, and had fewer infiltra
102 d integration site) signaling and regulating smooth muscle cell survival, as well as differentiation
106 Activated CD4 T cells connect to airway smooth muscle cells (ASMCs) in vitro via lymphocyte-deri
108 portant in regulating healthy primary airway smooth muscle cells (ASMCs), whereas changed expression
111 o, knockdown of T-cadherin from human aortic smooth muscle cells (HASMCs) with synthetic phenotype si
117 stressful conditions, pulmonary artery (PA) smooth muscle cells (PASMCs) exhibit a "cancer-like" pro
119 , the role of HIF-1alpha in pulmonary artery smooth muscle cells (PASMCs) remains controversial.
120 ute to the proliferation of pulmonary artery smooth muscle cells (PASMCs), and inhibition of phosphod
123 because voltage-dependent Ca(2+) channels in smooth muscle cells (SMC) provide the Ca(2+) that trigge
124 BB)-stimulated proliferation of human venous smooth muscle cells (SMC) was measured by a DNA-binding
126 es, inhibited proliferation and migration of smooth muscle cells (SMCs) and promoted the tube formati
128 he Rho GTPase-activating protein ARHGAP42 in smooth muscle cells (SMCs) controls blood pressure by in
134 A microarrays on the phenotypically distinct smooth muscle cells (SMCs) within the rat anorectrum, we
135 demonstrated TLR7 expression in macrophages, smooth muscle cells (SMCs), and endothelial cells from m
136 expression of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype coul
139 OCs) in proliferative and migratory vascular smooth muscle cells (VSMCs) are quite intricate with man
140 ions (AJ) along the borders between vascular smooth muscle cells (VSMCs) in the pressurized rat super
143 Proliferation and migration of vascular smooth muscle cells (VSMCs) or endothelial cell (ECs) pr
144 MicroRNAs are key regulators of vascular smooth muscle cells (VSMCs) phenotypic switch, one of th
147 apurinic/apyrimidinic endonuclease I protect smooth muscle cells against oxidant-induced cell death.
148 ts due to this ACTA2 mutation in both aortic smooth muscle cells and adventitial fibroblasts may cont
149 II (30 nm) also increased TRPM4 currents in smooth muscle cells and constricted cerebral arteries fr
150 hritis, IL-26 is expressed by renal arterial smooth muscle cells and deposits in necrotizing lesions.
151 nternalized by endothelial cells relative to smooth muscle cells and fibroblasts, demonstrating a dir
152 the major KV1 channel expressed in vascular smooth muscle cells and is abundantly localized on the p
156 th muscle alpha-actin filaments in wild-type smooth muscle cells by various mechanisms activates nucl
157 revealed that the origin of aortic vascular smooth muscle cells can be traced back to progenitor cel
158 real-time imaging was performed in vascular smooth muscle cells expressing a FRET-biosensor comprisi
161 teins and cocaine was confirmed in pulmonary smooth muscle cells from cocaine injected HIV-transgenic
164 this study was to determine whether vascular smooth muscle cells in cultured microvascular networks m
165 e of the ischemic cascade: selective loss of smooth muscle cells in juveniles but not adults shortly
166 x18 selectively marks pericytes and vascular smooth muscle cells in multiple organs of adult mouse.
170 on of smooth muscle alpha-actin filaments in smooth muscle cells increases reactive oxygen species le
172 ies revealed that loss of YY1AP1 in vascular smooth muscle cells leads to cell cycle arrest with decr
173 c increase in the proliferation of pulmonary smooth muscle cells on exposure to HIV-proteins and/or c
174 orylated SMAD2/3 in human pulmonary arterial smooth muscle cells on treatment with cocaine and Tat.
175 n and pharmacological inhibition in vascular smooth muscle cells reveal that cytochrome b5 reductase
176 aorta establishes the long-lived lineages of smooth muscle cells that make up the wall of the adult a
177 nted Sox10(+) stem cells differentiated into smooth muscle cells to stabilize functional microvessels
184 hus potentiating AngII signaling in vascular smooth muscle cells without an increase in the exogenous
185 erformed on two cell lines: A7r5 (rat aortic smooth muscle cells) and SH-SY5Y (human neuroblastoma ce
187 luripotent stem cell-derived cardiomyocytes, smooth muscle cells, and endothelial cells (in a 2:1:1 r
188 hen seeded the scaffold with cardiomyocytes, smooth muscle cells, and endothelial cells that had been
189 odest reduction of proliferation in vascular smooth muscle cells, but given low proliferative capacit
193 ells, which encompass pericytes and vascular smooth muscle cells, is a hallmark of CADASIL and other
194 om different origins, including endothelial, smooth muscle cells, macrophages, hepatocytes, adipocyte
196 hat neoarterioles were aberrantly covered by smooth muscle cells, with increased interprocess spacing
212 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of enhanced
215 pidly activated RhoA, ERK, and Akt in airway smooth-muscle cells, but only in the presence of TSG-6.
216 pithelial ion transport and fluid secretion, smooth muscle constriction, neuronal excitability, and c
219 tro approach for studying characteristics of smooth muscle contractility even though this experimenta
220 ss, but how they interact to regulate airway smooth muscle contractility is not fully understood.
221 enzyme expression, endothelial dysfunction, smooth muscle contractility, and vascular remodeling.
222 hose vascular effects include stimulation of smooth muscle contractility, migration, and proliferatio
225 a vital mechanism for the control of airway smooth muscle contraction and thus are a critical factor
226 congenital disorder characterized by loss of smooth muscle contraction in the bladder and intestine.
228 latory light chain (RLC) phosphorylation for smooth muscle contraction with subsequent dephosphorylat
229 oded by TMEM16A control neuronal signalling, smooth muscle contraction, airway and exocrine gland sec
230 n, transforming growth factor-beta, vascular smooth muscle contraction, and the hedgehog and Wnt sign
231 ching morphogenesis, the frequency of airway smooth muscle contraction, and the rate of developmental
232 , and identified distinct pathways linked to smooth muscle contraction, inflammatory cytokines, immun
236 In contrast, microanastomosis leads to early smooth muscle death and subsequent colonization of the v
239 lso found that TSPAN2 is highly expressed in smooth muscle-enriched tissues and down-regulated in in
240 by promoting monocyte firm adhesion, whereas smooth muscle EphA2 expression may regulate the progress
242 nic hedgehog expression, leading to aberrant smooth muscle formation and defective contraction of the
243 airment in BKCa channel function in vascular smooth muscle from diabetic patients through unique mech
244 similar alterations occur in native vascular smooth muscle from humans with type 2 diabetes is unclea
245 tudy, we evaluated BKCa function in vascular smooth muscle from small resistance adipose arteries of
252 lar matrix, which enhanced subsequent airway smooth muscle growth by 1.5-fold (P < 0.05), which was d
254 sthma, mast cells are associated with airway smooth muscle growth, MMP-1 levels are associated with b
256 e thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased angiogenesis.
257 Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF-beta1/SM
258 RATIONALE: Mutations in ACTA2, encoding the smooth muscle isoform of alpha-actin, cause thoracic aor
259 nslocation and Rho-kinase activity in airway smooth muscle largely via ARHGEF1, but independently of
261 ion of extracellular matrix (ECM) and larger smooth muscle mass are correlated with increased airway
262 ated features of airway remodeling including smooth muscle mass, extracellular matrix deposition and
264 selective genetic deletion of melanopsin in smooth muscle mostly removed the light-induced, but not
265 showed that the interaction between CBFbeta-smooth muscle myosin heavy chain (SMMHC; encoded by CBFB
269 with highest expression in the purely phasic smooth muscle of anococcygeus (ASM) vs. the truly tonic
273 compartment that began to express markers of smooth muscle precursors and adventitial fibrocytes, res
274 ifferentiation and proliferation of ureteric smooth muscle progenitor cells during murine kidney-uret
276 on to advanced atherosclerosis by regulating smooth muscle proliferation and extracellular matrix dep
277 ast cell numbers were associated with airway smooth muscle proliferation and MMP-1 protein associated
278 hetic phenotype, and EphA2 depletion reduces smooth muscle proliferation, mitogenic signaling, and ex
279 tion of the endothelium coordinates vascular smooth muscle relaxation along resistance arteries durin
280 y activated by cAMP (Epac), induces vascular smooth muscle relaxation by increasing the activity of r
287 bular maturation, and the differentiation of smooth muscle, renin, and mesangial cells were impaired.
289 of non-muscle (NM) isoforms of myosin II in smooth muscle (SM) tissues and their possible role in co
290 ization of freshly dispersed ICC and colonic smooth muscles, suggesting that this conductance is acti
291 mmalian cells, including epithelia, vascular smooth muscle tissue, electrically excitable cells, and
293 muscle (SM) myosin II are both expressed in smooth muscle tissues, however the role of NM myosin in
295 otype, EphA2 shows enhanced expression after smooth muscle transition to a synthetic phenotype, and E
297 antly influencing the phenotypic tonicity in smooth muscle via ROCK2: a lack of tone in ASM may be as
298 E: Decreasing Ca(2+) sensitivity of vascular smooth muscle (VSM) allows for vasodilation without lowe
299 crease phosphorylation of myosin in vascular smooth muscle (VSM) cells, causing persistent constricti
300 ay inflammation, mucus, fibrosis, and airway smooth muscle were no different in Ormdl3(Delta2-3/Delta
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