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1  a role of EphB2 and its ligands in vascular smooth muscle cell proliferation.
2 molecular-weight forms of hyaluronan inhibit smooth muscle cell proliferation.
3 nflammation, lipid accumulation and vascular smooth muscle cell proliferation.
4 elet-derived growth factor (PDGF)-stimulated smooth muscle cell proliferation.
5 tional signaling cascade leading to vascular smooth muscle cell proliferation.
6 ective as apoE in inhibiting PDGF-stimulated smooth muscle cell proliferation.
7 prostaglandin E(2), an inhibitor of vascular smooth muscle cell proliferation.
8  thrombin production, blood coagulation, and smooth muscle cell proliferation.
9 bit an NO-independent inhibition of vascular smooth muscle cell proliferation.
10      Paclitaxel is known to inhibit vascular smooth muscle cell proliferation.
11 ning to total vascular lumen blockade due to smooth muscle cell proliferation.
12 p14) and CDKN2B (p15) and increased vascular smooth muscle cell proliferation.
13 and ischemia and causes vasoconstriction and smooth muscle cell proliferation.
14 EC proliferation but stimulated pericyte and smooth muscle cell proliferation.
15 rin and cell surfaces, and as a stimulus for smooth muscle cell proliferation.
16 as been shown to inhibit thrombin-stimulated smooth muscle cell proliferation.
17 te and platelet activation and by inhibiting smooth muscle cell proliferation.
18 directly or indirectly, and also in inducing smooth muscle cell proliferation.
19      In addition, estrogen inhibits vascular smooth muscle cell proliferation.
20 n promotes inflammatory cell recruitment and smooth muscle cell proliferation.
21 a permissive, if not facilitatory, impact on smooth muscle cell proliferation.
22 vessel wall injury during periods of maximal smooth muscle cell proliferation.
23 hatase, MAP kinase phosphatase-1 (MKP-1), in smooth muscle cell proliferation.
24 oth muscle contractility and small intestine smooth muscle cell proliferation.
25 al wall thickening because of suppression of smooth muscle cell proliferation.
26 oplasty can result in apoptosis and vascular smooth muscle cell proliferation.
27 racterized by prominent endothelial cell and smooth muscle cell proliferation.
28 been implicated in mitosis, cytokinesis, and smooth muscle cell proliferation.
29 clear antigen (PCNA), important mediators of smooth muscle cell proliferation.
30 ctive at inhibiting leiomyoma and myometrial smooth muscle cell proliferation.
31 ion/activation as well as with inhibition of smooth muscle cell proliferation.
32 ing medial area, proteoglycan deposition, or smooth muscle cell proliferation.
33  antiplatelet agent that suppresses vascular smooth muscle cell proliferation.
34 ally reduced epidermal growth factor-induced smooth muscle cell proliferation.
35 the mechanism whereby diabetes may stimulate smooth muscle cell proliferation.
36 etaVLDL-induced signaling pathway results in smooth muscle cell proliferation.
37 noncavitational ultrasound energy may impact smooth muscle cell proliferation.
38 ve metabolism, cytosolic calcium, and ductal smooth muscle cells proliferation.
39 tial role in angiotensin II-induced vascular smooth muscle cell proliferation, 2) JAK2 plays an essen
40                        MMF inhibits arterial smooth muscle cell proliferation, a contributor to graft
41 iously that homocysteine stimulates vascular smooth muscle cell proliferation, a hallmark of arterios
42       The low efficiency of apoE4 to inhibit smooth muscle cell proliferation also suggested another
43 y and enhancer of Split-5 (HES-5) protein to smooth muscle cell proliferation and a shift to an undif
44 een immune and nonimmune factors, leading to smooth muscle cell proliferation and accumulation in the
45 egard to the potential role of GD3 in aortic smooth muscle cell proliferation and apoptosis that may
46 signaling, collagen production, and vascular smooth muscle cell proliferation and calcification in vi
47  by Ca(v)3.x genes, control pulmonary artery smooth muscle cell proliferation and cell cycle progress
48 on, enhanced macrophage recruitment, reduced smooth muscle cell proliferation and collagen content, a
49 anulation tissue development, and ultimately smooth muscle cell proliferation and extracellular matri
50 Serotonin (5-HT) stimulates pulmonary artery smooth muscle cell proliferation and has been associated
51 eptor signaling is implicated in controlling smooth muscle cell proliferation and in maintaining smoo
52 vascular injury, but still inhibits vascular smooth muscle cell proliferation and increases uterine w
53  vasculoprotective effect of NOD by reducing smooth muscle cell proliferation and inflammation-induce
54    We found that IFN-gamma-mediated vascular smooth muscle cell proliferation and intimal expansion w
55 a suggest that T. cruzi infection stimulates smooth muscle cell proliferation and is likely a result
56 c hypoxia causes pulmonary hypertension with smooth muscle cell proliferation and matrix deposition i
57 s to ET(A) receptors, it stimulates vascular smooth muscle cell proliferation and may thus be pivotal
58 ecrosis factor family of receptors, promotes smooth muscle cell proliferation and migration and may a
59  macrolide antibiotic that inhibits vascular smooth muscle cell proliferation and migration and that
60 The TZD troglitazone (TRO) inhibits vascular smooth muscle cell proliferation and migration both in v
61  growth factor-I (IGF-I) stimulates vascular smooth muscle cell proliferation and migration by activa
62                              SCPEP1 promotes smooth muscle cell proliferation and migration in a cata
63                  Similarly, MSC(CM) promoted smooth muscle cell proliferation and migration in a dose
64 Sunitinib decreased neointimal formation and smooth muscle cell proliferation and migration in a dose
65                 Paclitaxel prevents vascular smooth muscle cell proliferation and migration in vitro
66 attenuate tenascin-C expression and vascular smooth muscle cell proliferation and migration in vitro.
67 ot a catalytic triad mutant SCPEP1, promotes smooth muscle cell proliferation and migration in vitro.
68 al hyperplasia, a lesion generated by medial smooth muscle cell proliferation and migration into the
69                       Aberrant regulation of smooth muscle cell proliferation and migration is associ
70                                              Smooth muscle cell proliferation and migration is import
71 t macrophages less potently induced vascular smooth muscle cell proliferation and migration than that
72                      IGFs stimulate vascular smooth muscle cell proliferation and migration to form t
73 ct against endothelial dysfunction, vascular smooth muscle cell proliferation and migration, and modu
74 hibitor 1, endothelial dysfunction, vascular smooth muscle cell proliferation and migration, apoptosi
75 ne to investigate the effect of sunitinib on smooth muscle cell proliferation and migration.
76 small G protein Rho is required for vascular smooth muscle cell proliferation and migration.
77 chymal growth factors capable of stimulating smooth muscle cell proliferation and migration.
78 he absence of ApoE and functions to increase smooth muscle cell proliferation and migration.
79 mation and oxidative stress, inhibiting also smooth muscle cell proliferation and migration.
80 d role of fbln-5 as an inhibitor of vascular smooth muscle cell proliferation and migration.
81 ntitumor activity, has been shown to inhibit smooth muscle cell proliferation and migration.
82 et-derived growth factor- (PDGF-) stimulated smooth muscle cell proliferation and migration.
83 conclude that BNP potently inhibits vascular smooth muscle cell proliferation and potentiates the gen
84 on, we confirmed that treprostinil inhibited smooth muscle cell proliferation and prevented progressi
85 nd systemic circulation and reduced vascular smooth muscle cell proliferation and redox-sensitive gen
86 sults identify SMILR as a driver of vascular smooth muscle cell proliferation and suggest that modula
87      This correlated with decreased vascular smooth muscle cell proliferation and survival, decreased
88 llow viral infections with subsequent airway smooth muscle cell proliferation and the formation of an
89                      Chronic hypoxia induces smooth muscle cell proliferation and vessel wall remodel
90  peroxide (H(2)O(2)), in modulating vascular smooth muscle cell proliferation and viability is contro
91 t influenza infection promotes inflammation, smooth muscle cell proliferation, and fibrin deposition
92 denced by the disruption of elastic laminae, smooth muscle cell proliferation, and focal endothelial
93  developed less neointimal hyperplasia, less smooth muscle cell proliferation, and had fewer infiltra
94 elial tubulogenesis, paracrine regulation of smooth muscle cell proliferation, and hematopoiesis.
95 l functions, including platelet aggregation, smooth muscle cell proliferation, and immune regulation.
96 lerosis (TVS) is characterized by neointimal smooth muscle cell proliferation, and is driven by both
97 droxyestrone provoked human pulmonary artery smooth muscle cell proliferation, and this mitogenic eff
98  development of hypoxia-induced PH, vascular smooth muscle cell proliferation, and vascular remodelin
99                                              Smooth muscle cell proliferation around small pulmonary
100 attenuated balloon injury-induced neointimal smooth muscle cell proliferation as determined by bromod
101       At 28 days, there was no difference in smooth muscle cell proliferation as measured by the prol
102                                 CO inhibited smooth muscle cell proliferation by activating p38 mitog
103 ostanoid prostacyclin (PGI2) inhibits aortic smooth muscle cell proliferation by blocking cell cycle
104 PARgamma ligands inhibit rat aortic vascular smooth muscle cell proliferation by blocking the events
105                                Inhibition of smooth muscle cell proliferation by NO has been document
106  cell cycle-dependent inhibition of arterial smooth muscle cell proliferation by progesterone may rep
107 HS isolated from HDL-treated cells inhibited smooth muscle cell proliferation (by 83 +/- 5%) better t
108 artery supports the hypothesis that abnormal smooth muscle cell proliferation caused by ACTA2 mutatio
109 therosclerotic lesion formation by affecting smooth muscle cell proliferation, collagen deposition, a
110                                     Although smooth muscle cell proliferation contributes to the vasc
111 tae demonstrated that MIF deficiency reduced smooth muscle cell proliferation, cysteine protease expr
112 vation and enhanced coagulability, increased smooth muscle cell proliferation, cytotoxicity, inductio
113 n of which is associated with rapid vascular smooth muscle cell proliferation during development.
114    Despite inhibition of underlying vascular smooth muscle cell proliferation, E2F decoy oligonucleot
115 utic application for selective inhibition of smooth muscle cell proliferation, enhancement of endothe
116 raft inflammatory cell infiltration, intimal smooth muscle cell proliferation, fibrosis, and elastic
117 een documented to include decreased vascular smooth muscle cell proliferation following decreased ERK
118 ased serotonin and promoted pulmonary artery smooth muscle cell proliferation in a serotonin-dependen
119 f this study was to detect coronary vascular smooth muscle cell proliferation in a swine model by ima
120 K2, thereby contributing to the induction of smooth muscle cell proliferation in atherosclerosis.
121                          Enoxaparin inhibits smooth muscle cell proliferation in experimental models.
122  relationship between glucose metabolism and smooth muscle cell proliferation in IPAH.
123    PHD2-deficient endothelial cells promoted smooth muscle cell proliferation in part through hypoxia
124 inases JAK2, MEK1, and ERK1 mediate vascular smooth muscle cell proliferation in response to both gro
125 dies against MEK1 or ERK1 abolished vascular smooth muscle cell proliferation in response to either p
126 ffects on endothelial cell (EC) and vascular smooth muscle cell proliferation in rodent models of car
127 racterized by excessive vascular resistance, smooth muscle cell proliferation in small pulmonary arte
128                                              Smooth muscle cell proliferation in the injured wall, me
129    One possibility is that DNA damage causes smooth muscle cell proliferation in the intima of arteri
130 n induce both endothelial cell apoptosis and smooth muscle cell proliferation in the systemic circula
131 himeric hammerhead ribozyme to PCNA inhibits smooth muscle cell proliferation in vitro and reduces bo
132     The nanoparticles inhibited human aortic smooth muscle cell proliferation in vitro and showed gre
133 viously been demonstrated to be required for smooth muscle cell proliferation in vitro, the role of t
134 uced endothelial shear stress and stimulates smooth muscle cell proliferation in vitro.
135 expression, which induced pulmonary arterial smooth muscle cell proliferation, in the lungs of these
136 atios were significantly correlated with the smooth muscle cell proliferation index (r2 = 0.528, P <
137                                            A smooth muscle cell proliferation index of 30 was used as
138                                            A smooth muscle cell proliferation index, calculated as (B
139 ies inhibits vascular activation, preventing smooth muscle cell proliferation, intimal hyperplasia, a
140                                     Abnormal smooth muscle cell proliferation is a primary hallmark o
141 nted that apoE inhibition of PDGF-stimulated smooth muscle cell proliferation is mediated by its bind
142 revious data showing that apoE inhibition of smooth muscle cell proliferation is mediated through its
143                                     In situ, smooth muscle cell proliferation (Ki67) was not influenc
144 nstrictor, inducer of fibrosis, and vascular smooth muscle cell proliferation, may play a key role in
145 xpansion after arterial injury and decreased smooth muscle cell proliferation, migration, and express
146 ooth muscle cells, which is known to promote smooth muscle cell proliferation, migration, and IH, but
147 n was arterial intimal thickening comprising smooth muscle cell proliferation, mononuclear cell infil
148 ld to moderate asthma may result from airway smooth muscle cell proliferation or acquisition of a hyp
149 panel of growth factors (GFs) known to alter smooth muscle cell proliferation or migration.
150 ritical regulatory sites that mediate airway smooth muscle cell proliferation or modulate cell adhesi
151 apoE also suppressed PDGF- and oxLDL-induced smooth muscle cell proliferation (p < 0.001).
152  been highlighted, such as the inhibition of smooth muscle cell proliferation, preservation of endoth
153  that also inhibits platelet aggregation and smooth muscle cell proliferation, properties that may pr
154 del of megacolon that results from increased smooth muscle cell proliferation rather than altered neu
155 hus identified showed efficacy in inhibiting smooth muscle cell proliferation relative to catalytical
156  the T-antigen transgenic mice the increased smooth muscle cell proliferation results in thickening o
157 otent at increasing vascular endothelial and smooth muscle cell proliferation than bolus administrati
158 Although mechanical vascular injury leads to smooth muscle cell proliferation that contributes to res
159  of unknown etiology consisting of lymphatic smooth muscle cell proliferation that results in the obs
160 hickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were sig
161  vascular resistance and attenuates vascular smooth muscle cell proliferation through signal transduc
162 s associated with increased pulmonary artery smooth muscle cell proliferation via enhanced AT(1) rece
163 sylceramide (LacCer) stimulated human aortic smooth muscle cell proliferation via specific activation
164 1), serotonin can mediate pulmonary arterial smooth muscle cell proliferation via the serotonin trans
165  betaVLDL-induced activation of ERK1/ERK2 to smooth muscle cell proliferation was also explored.
166                                              Smooth muscle cell proliferation was assessed using brom
167               Greater than 50% inhibition of smooth muscle cell proliferation was observed at 15 micr
168 s (ROS) have been implicated as mediators of smooth muscle cell proliferation, we hypothesized that i
169        Increases in vascular medial area and smooth muscle cell proliferation were quantified followi
170 mpound 6c inhibited PDGF-stimulated vascular smooth muscle cell proliferation with an IC50 of 0.3 mic
171                      Increased hypercellular smooth muscle cell proliferation with exaggerated intima
172 th muscle cells in vivo results in increased smooth muscle cell proliferation without de-differentiat
173 ium-binding protein associated with vascular smooth muscle cell proliferation, would be associated wi

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