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1 -positive cells were present within arterial neointima.
2 ing for proteomics analysis of the media and neointima.
3 lar smooth muscle cells within the expanding neointima.
4 h control by measuring degree of stenosis by neointima.
5 g and significantly decreased injury-induced neointima.
6 wed by balloon overstretch of the developing neointima.
7 on in cells of the vascular tunica media and neointima.
8 the regenerating endothelium, but not in the neointima.
9 matrix deposition, and formation of a thick neointima.
10 adventitia and by smooth muscle cells of the neointima.
11 on of vascular smooth muscle cells to form a neointima.
12 iferate and migrate from the media to form a neointima.
13 r endothelial growth factor failed to elicit neointima.
14 ts, with struts being sequestered within the neointima.
15 increased hyaluronan (HA) deposition in the neointima.
19 contrast, VSMC-derived cells generating the neointima after vascular injury generally retained the e
20 n in the number of LacZ labeled cells in the neointima after vascular injury, concomitant with reduce
22 bstantial infiltration of macrophages in the neointima and adventitia of the ligated left carotid art
24 ntial for accumulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the ad
30 ha-smooth muscle actin positive cells in the neointima) and endothelial activation (increased P-selec
36 s, existing smooth muscle cells give rise to neointima, but on extensive damage, they are replaced by
37 level of p27(kip1) located in the nucleus of neointima cells in SGK-1 knockout mice compared with tha
38 ), and psiepsilonRACK significantly promoted neointima development (32.4+/-4.9%, P=0.033), whereas ep
42 n atherosclerotic plaques and injury-induced neointima did not contain VSMC-derived cells expressing
43 (monocytes, macrophages, lymphocytes) in the neointima did not differ among the different CRPtg genot
44 +) MSC-like cells migrate into the media and neointima during athero- and arteriosclerosis in ApoE(-/
45 sion to 35% of uninjured controls, inhibited neointima formation (>70%), inhibited VSM proliferation
47 ited cell proliferation and markedly reduced neointima formation 14 days post injury; similar results
48 d compound transgenic mice were resistant to neointima formation 21 days after carotid injury and sho
51 t that platelet CD40 plays a pivotal role in neointima formation after arterial injury and might repr
52 However, the direct impact of platelets on neointima formation after arterial injury remains undete
53 let-leukocyte activation and recruitment and neointima formation after arterial injury, potentially t
57 t LXR ligands inhibit VSMC proliferation and neointima formation after balloon injury and suggest tha
58 study was to determine the role of Orai1 in neointima formation after balloon injury of rat carotid
59 Orai3 potential upregulation and role during neointima formation after balloon injury of rat carotid
62 femoral cuff injury whereas hPBMCs promoted neointima formation after carotid wire injury 4 weeks af
63 nstituted mice, hPBMC reconstitution reduced neointima formation after femoral cuff injury whereas hP
64 in high-fat diet-induced atherosclerosis and neointima formation after injury in atherosclerosis-pron
66 BMDCs alone was necessary and sufficient for neointima formation after vascular injury and provide ev
68 y provide strong evidence that asTF promotes neointima formation and angiogenesis in an experimental
70 of iPLA(2)beta exacerbates ligation-induced neointima formation and enhanced both production of proi
71 inker protein, was shown to be essential for neointima formation and for p38 mitogen-activated protei
73 entiviral particles encoding shRNA inhibited neointima formation and inward and outward vessel remode
74 based, paclitaxel-eluting stents on in-stent neointima formation and late incomplete stent apposition
75 w that genetic deficiency of Cxcr7 increased neointima formation and lesional macrophage accumulation
77 hat estrogen (17beta-estradiol; E2) inhibits neointima formation and migration of leukocytes, particu
79 , asTF gene transfer significantly increased neointima formation and neovascularization after carotid
80 ied the effects of Epac1 null by suppressing neointima formation and proliferative VSMC accumulation
81 s as critical cellular effectors of Nf1(+/-) neointima formation and propose a potential therapeutic
82 R2 expression effectively inhibited Nf1(+/-) neointima formation and reduced macrophage content in th
83 scular smooth muscle cells and contribute to neointima formation and repair after acute injury to the
84 rly progression of vascular inflammation and neointima formation and suggest that iPLA(2)beta may rep
85 of IL-1beta signaling in mediating arterial neointima formation and suggest the involvement of IL-1
86 or for the proliferative response underlying neointima formation and target genes trans-activated by
87 ubstrate 2 alpha) in mice profoundly reduces neointima formation and vascular remodelling following c
91 rial injury (P<0.05), resulting in decreased neointima formation at 4 weeks compared with control (P<
92 In mice, ETS-DN, but not ETS-MU, reduced neointima formation at days 7 and 21 and reduced the exp
93 Rac1, but not Vav2, also is important for neointima formation but not for hypertension-driven vasc
96 on Nf1(+/-) neointima formation, we induced neointima formation by carotid artery ligation in Nf1(+/
97 ARgamma is both necessary and sufficient for neointima formation by components of oxidized low densit
98 suggest that KIS protects against excessive neointima formation by opposing stathmin-mediated VSMC m
100 odel, Tsc2(+/-) mice significantly increased neointima formation compared with the control mice, and
101 IL8RB-EC, and IL8RA/RB-EC treatment reduced neointima formation dramatically (by 80%, 74%, and 95%)
103 ole of the human immune system on subsequent neointima formation elicited by vascular injury in a hum
107 d for NFAT activity, VSMC proliferation, and neointima formation following balloon injury of rat caro
108 proliferation, and also markedly accentuates neointima formation following rat carotid angioplasty.
109 cate that ROCK1 in BM-derived cells mediates neointima formation following vascular injury and sugges
110 phy following monocrotaline and in rats with neointima formation following VEGF receptor blockade and
112 topical application of MCV1 markedly reduced neointima formation in a mouse model of restenosis.
114 nvolvement of these transcription factors in neointima formation in a rat carotid artery balloon inju
115 rowth and survival and may contribute to the neointima formation in atherosclerosis and restenosis.
116 ts unveil the role of ETS-1 as a mediator of neointima formation in AVF and may result in the develop
117 d surface, thus suppressing inflammation and neointima formation in balloon-injured rat carotid arter
118 retard development of glomerulosclerosis and neointima formation in chronic transplant dysfunction.
119 Likewise, RNase1 administration reduced neointima formation in comparison with vehicle-treated A
120 which is a signaling axis directly linked to neointima formation in diverse animal models of vasculop
123 ed arterial injury, we demonstrate decreased neointima formation in NOR1(-/-) mice compared with wild
125 At 21 days after ferric chloride injury, neointima formation in P2Y(12)(-/-) arteries was signifi
129 investigated the role of elevated sCD40L in neointima formation in response to vascular injury in an
131 d demonstrate that NOR1 deficiency decreases neointima formation in response to vascular injury.
132 ollowing this intervention, we found reduced neointima formation in Rock1(+/-) mice compared with tha
135 1beta overexpression substantially inhibited neointima formation in vivo and markedly inhibited VSMC
136 roliferation in vitro and for injury-induced neointima formation in vivo by modulating Rac1-NFATc1-cy
144 gly suggest that the severity of age-related neointima formation is primarily determined by the recip
145 ter treatment of carotids with PDGF and that neointima formation is significantly reduced in carotids
146 media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of
147 ells is sufficient to reproduce the enhanced neointima formation observed in Nf1(+/-) mice when compa
154 monstrate that NFATs play a critical role in neointima formation via induction of expression of COX-2
155 Luminal occlusion of the graft caused by neointima formation was 29.3+/-19.4% (n=5) after transfe
158 IFN-gammaR-deficient recipients and in which neointima formation was induced by intravenous administr
159 tion compared with the control mice, and the neointima formation was inhibited by treatment with rapa
162 unction, invasion of inflammatory cells, and neointima formation were suppressed in mice with heteroz
164 (VEGF)-2 could achieve similar reductions in neointima formation while accelerating, rather than inhi
165 ic SENP1 knockout grafts demonstrate limited neointima formation with attenuated leukocyte recruitmen
167 Nox4 inhibits oxidation of SERCA, as well as neointima formation, after ZO common carotid artery inju
168 model, AIP1 deletion in the graft augmented neointima formation, an effect reversed in AIP1/interfer
169 he mechanism by which p38alpha MAPK promotes neointima formation, an in vitro SMC culture system was
170 injury influenced endothelial regeneration, neointima formation, and homing of human inflammatory an
171 during the proliferative response underlying neointima formation, and this transcriptional induction
172 aortic graft injury model promotes extensive neointima formation, as shown by optical coherence tomog
173 osis is characterized in part by exaggerated neointima formation, but the underlying mechanism remain
174 nd angiogenic factors in atherosclerosis and neointima formation, emphasizing the problems raised by
176 inhibit SMC proliferation and injury-induced neointima formation, induced SMC redifferentiation.
177 SMC p38alpha MAPK activation is required for neointima formation, perhaps because of its ability to p
178 h muscle-specific iPLA(2)beta is involved in neointima formation, we generated transgenic mice in whi
179 gate the role of CCR2 activation on Nf1(+/-) neointima formation, we induced neointima formation by c
180 al role of fbln-5 in vascular remodeling and neointima formation, we induced vascular injury by carot
181 rmine the role of leukocyte-derived ROCK1 in neointima formation, we performed reciprocal bone marrow
182 including inflammatory cell recruitment and neointima formation, were markedly inhibited by PRT06031
183 smooth muscle cells leads to characteristic neointima formation, which can be exacerbated by genetic
184 Injection of wild-type platelets promoted neointima formation, which was associated with increased
235 of AMPKalpha in the development of vascular neointima hyperplasia and to elucidate the underlying me
236 odel of vascular injury, we observed reduced neointima hyperplasia in Quaking viable mice, which have
241 rterial injury and IGF-1R phosphorylation in neointima increased significantly in LAR(-/-) mice compa
242 nly genome-wide association studies of human neointima-induced in-stent stenosis confirmed the associ
245 d CamKIIdelta2 upregulation in the media and neointima; inhibited cell proliferation and markedly red
247 oth Muscle Cell (VSMC) migration into vessel neointima is a therapeutic target for atherosclerosis an
249 ormation when the proliferative index of the neointima is highest and that Id3 promotes smooth muscle
254 of the smooth muscle cells captured from the neointima lesion by laser capture microdissection at 16
255 ry system produces substantial mitigation of neointima, likely due to its favorable physical properti
256 presence of large necrotic cores within the neointima may be associated with the inability of the ve
258 1(+/+) marrow both had significantly reduced neointima/media compared with IL-1R1(+/+) to IL-1R1(+/+)
261 /+) (P < 0.05) but had significantly greater neointima/media than IL-1R1(-/-) to IL-1R1(-/-) controls
262 modeled pulmonary arteries, ie, endothelium, neointima, medial smooth muscle, and adventitia, in the
264 rafts fail within 10 years after CABG due to neointima (NI) formation, a process involving the prolif
265 Epac1 gene led to a significant reduction in neointima obstruction in response to vascular injury.
266 ve coronary angiography, with an increase in neointima of 0.68+/-0.43 mm(2) on optical coherence tomo
270 g coronary vessels, LPP was expressed in the neointima of cells lacking smoothelin and showed express
271 munohistochemistry revealed human CRP in the neointima of CRPtg, but little or none was observed in t
274 ifferentiate into smooth muscle cells in the neointima of injured arteries, we hypothesized that the
276 rated increased heparanase expression in the neointima of obese, hyperlipidemic rats in comparison to
277 n-like protein (ESDN) is up-regulated in the neointima of remodeling arteries and modulates vascular
278 rate through an irradiated vein graft to the neointima of the vessel and transdifferentiate to expres
279 via low density lipoprotein retention in the neointima of vessels due to binding with modified proteo
280 a novel gene expressed in the adventitia and neointima on arterial injury and found that it functiona
286 e extent of heparanase expression within the neointima strongly correlated with the neointimal thickn
288 The targeted NP group resulted in lower neointima-to-media (N/M) scores at 2 wk versus control g
291 hich cell types contribute to the developing neointima, we established a novel mouse model of resteno
292 tidylinositol 3-kinase signaling in Nf1(+/-) neointimas, we tested the hypothesis that Ras-Erk signal
294 Young aortas invariably developed thicker neointima when transplanted into old recipients than whe
295 em/progenitor cells exists within developing neointima, which displays the ability to differentiate i
296 -) mice resulted in accelerated formation of neointima, which is composed predominantly of VSMCs.
297 /- mice resulted in accelerated formation of neointima, which is composed predominantly of VSMCs.
300 men at postprocedure rather than exaggerated neointima within the stent or plaque proliferation at th
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