ライフサイエンスコーパス: aortic ring

1 ons with vessels that have sprouted from rat aortic rings.

2 GABA had no relaxing effect on rat aortic rings.

3 b) at stimulating relaxation of isolated rat aortic rings.

4 neous angiogenic response of freshly cut rat aortic rings.

5 ormance, and impaired vascular relaxation of aortic rings.

6 ic acid, was markedly increased in apoE(-/-) aortic rings.

7 endothelium-dependent relaxant responses of aortic rings.

8 tube formation on Matrigel, and sprouting of aortic rings.

9 e-precontracted endothelium-denuded thoracic aortic rings.

10 e cells (SMCs), and on contraction in rabbit aortic rings.

11 constriction in isolated endothelium-denuded aortic rings.

12 n isolated rat pulmonary artery and thoracic aortic rings.

13 r kallikrein, induced vascular relaxation of aortic rings.

14 essed using norepinephrine precontracted rat aortic rings.

15 segments and reduced Phe-induced response in aortic rings.

16 production and vessel relaxation in isolated aortic rings.

17 onduit and resistance vasculature by ex vivo aortic rings.

18 es and producing vasorelaxing effects on rat aortic rings.

19 ased protein glutathiolation in isolated rat aortic rings.

20 ion produced significant force generation in aortic rings.

21 In rat aortic rings, 17 beta-estradiol inhibited the increase o

22 ivity of rat endothelium-intact and -denuded aortic rings (2 mm) was studied ex vivo in a standard ti

23 n was greater in old (O) compared with Y rat aortic rings (60+/-6% versus 39+/-6%, P<0.05).

24 VEGF-induced microvessel sprouting from rat aortic ring and blood vessel formation in the Matrigel p

25 Analysis of endothelial sprouting in aortic ring and in vivo subcutaneous sponge assays from

26 EC migration and tube formation in vitro and aortic ring and Matrigel plug angiogenesis in vivo.

27 EC migration and tube formation in vitro and aortic ring and Matrigel plug angiogenesis in vivo.

28 SFLLRN contracted the endothelium-rubbed rat aortic rings and aggregated human platelets in vitro, wh

29 abbit femoral artery, and in vitro on rabbit aortic rings and cultured human umbilical vein endotheli

30 Vasodilation of rat aortic rings and formation of both NO gas and NO-modifie

31 Here, we used rat aortic rings and human umbilical vein endothelial cells

32 calcification in phosphate-treated VSMCs and aortic rings and in vitamin D3-treated mice.

33 physiological actions such as contraction of aortic rings and increase in BP was also observed in the

34 roduced a significant vascular reactivity in aortic rings and instantaneous and sustained vascular re

35 compounds evoked vasorelaxing effects on rat aortic rings and membrane hyperpolarization in human vas

36 S) gene, by studying isolated, precontracted aortic rings and mesenteric arterioles in situ.

37 A effectively inhibited the sprouts of mouse aortic rings and neoangiogenesis in chick embryo chorioa

38 ned PRA and SIM effects on vasorelaxation in aortic rings and NO production by cultured bovine aortic

39 suppression of microvessel outgrowth in rat aortic rings and rat cornea angiogenesis.

40 acetylcholine-induced relaxation of isolated aortic rings and resistance arteries.

41 media for vasoactive substances on isolated aortic rings and small-resistance arteries.

42 ects of DPI on GTN-induced relaxation of rat aortic rings and the function of purified ALDH2.

43 de, despite reduced contractile responses in aortic rings and the lack of effect on cardiac function.

44 d by Western blot for phosphorylated ERK1/2, aortic ring, and migration assays.

45 dothelial cells, ex vivo vessel outgrowth of aortic rings, and actual in vivo angiogenesis.

46 calcification in primary human VSMCs, rodent aortic rings, and rat A10 VSMC line.

47 Total RNA was harvested from the aortic rings, and reporter gene transcripts were quantif

48 ation, indicated by in vitro tube-formation, aortic-ring, and coated-bead assays and by in vivo coate

49 -derived, but not NO-induced, relaxations of aortic rings; and (iv) PQ-induced cytotoxicity is potent

50 quantitative three-dimensional ex vivo mouse aortic ring angiogenesis assays, in which developing mic

51 donor tissue and rabbit endothelium-denuded aortic ring as detector tissue, we report here that a va

52 The aortic ring assay allows analysis of cellular proliferat

53 alogues showing antiangiogenicity in the rat aortic ring assay also demonstrated antiproliferative ac

54 s-like tyrosine kinase-1 (sFlt-1) in both an aortic ring assay and a model of suture-induced corneal

55 GF receptor 2 and EphA signaling pathways in aortic ring assay and antiangiogenic efficacy of EphA2/F

56 nds to induce ex vivo vessel sprouting in an aortic ring assay and in vivo angiogenesis using a colla

57 locked the effects of U-II in vitro in a rat aortic ring assay and in vivo in a rat ear-flush model.

58 ed the length of vascular sprouts in the rat aortic ring assay and modulated VEGF-mediated tube forma

59 d bFGF-induced tube formation in an in vitro aortic ring assay and promoted bFGF-induced corneal angi

60 -13 inhibited capillary sprouting in the rat aortic ring assay and vessel growth in the Matrigel plug

61 analysis of functional activity using a rat aortic ring assay are discussed.

62 The aortic ring assay demonstrated that new vessels were pro

63 Further clinical and IHC analyses of the aortic ring assay indicated that TLR9 suppressed tip cel

64 Finally, ex vivo aortic ring assay to test the sprouting and microvessel

65 involved in vascular pH sensing, an ex vivo aortic ring assay was used under defined pH conditions.

66 ng, ELISA, enzyme immunoassay), ex vivo (rat aortic ring assay), and in vivo (chick chorioallantoic m

67 , 2) inhibition of tube formation in the rat aortic ring assay, 3) inhibition of VEGF- and bFGF-stimu

68 In the rat aortic ring assay, all 4 analogues in the N-substituted

69 L-4 inhibited capillary sprouting in the rat aortic ring assay, and vessel growth in the in vivo Matr

70 ited marginal inhibitory activity in the rat aortic ring assay, thereby demonstrating the requirement

71 pendent manner, microvessel formation in rat aortic ring assay, with inhibition reaching 76% at the h

72 ity to inhibit microvessel growth in the rat aortic ring assay.

73 sed endothelial cell sprouting in an ex vivo aortic ring assay.

74 ation) and inhibited angiogenesis in the rat aortic ring assay.

75 mation and sprouting of new vessels in a rat aortic ring assay.

76 nd display potent NO bioactivity in a rabbit aortic ring assay.

77 vo corneal angiogenesis model and an ex vivo aortic ring assay.

78 cket, tumor implantation) and in the ex vivo aortic ring assay.

79 Aortic ring assays reveal induced AnxA1 expression on sp

80 inhibited NE-induced vasoconstriction in rat aortic rings at micromolar concentration.

81 sustained vasodilation in precontracted rat aortic rings, attenuated coronary vasoconstriction in he

82 on, migration, capillary tube formation, and aortic ring-based angiogenesis.

83 ssociated vasoconstriction in an ex vivo rat aortic ring bioassay.

84 titive binding assay and ex vivo using a rat aortic ring bioassay.

85 cy (E(max)) of hUII and URP ex vivo in a rat aortic ring bioassay.

86 Expression of p56/Lck in murine aortic rings blocked sprouting angiogenesis.

87 ed phosphorylation of MEK1/2 and p38 MAPK in aortic rings, but not of NFkappaB.

88 tion of VEGF-stimulated sprouting from chick aortic rings by 65%, thus displaying a role in anti-angi

89 Relaxation of isolated aortic rings by kallistatin was observed in the presence

90 The effects of vasopressin on isolated aortic rings, cardiac function, mean arterial pressure,

91 in expression and function, vascular tone in aortic rings, cholesterol efflux from macrophages, and e

92 Abdominal aortic ring contraction experiments revealed that PGF2al

93 In isolated aortic rings, CORM-A1 promoted a gradual but profound co

94 17 beta-Estradiol-induced relaxation of rat aortic rings could not be prevented by cycloheximide or

95 Injured rat aortic rings cultured in collagen gels produced an angio

96 l plugs was absent from rap1a(-/-) mice, and aortic rings derived from rap1a(-/-) mice failed to spro

97 stimulated endothelial sprout formation from aortic rings dissected from WT but not from E-selectin-d

98 py of VEGF-, Ang-1, or VEGF/Ang-1-stimulated aortic rings double stained at time points of maximal ph

99 endothelium-dependent relaxations (EDRs) in aortic rings (ED50, 5.44+/-.18 versus 7.51+/-.10; P<.05)

100 nvolving HUVEC and/or HTR8 trophoblasts, and aortic ring endothelial cell outgrowth/sprouting.

101 ated endothelial NOS (eNOS) activity, and in aortic rings, endothelium-derived and eNOS-mediated rela

102 nduced a relaxation in preconstricted rabbit aortic rings ex vivo, thus mimicking acetylcholine-induc

103 er, 14d showed antiangiogenic activity in an aortic ring explant assay by blocking endothelial outgro

104 ibition of microvessel growth ex vivo in rat aortic ring explant cultures and in vitro on HUVEC capil

105 Ex vivo mutant aortic ring explants developed significantly fewer and t

106 apillary sprouting from annexin II-deficient aortic ring explants was markedly reduced in association

107 ion in HMEC-1 cells, angiogenic sprouting in aortic ring explants, and retinal revascularization in o

108 e of vascular hyporeactivity in rat thoracic aortic rings exposed to peroxynitrite.

109 e-precontracted endothelium-denuded thoracic aortic rings, exposure to LPS (10 ng/mL) in the presence

110 tery ligation and endothelial sprouting from aortic rings from adult miR-223(-/y) animals were enhanc

111 ations in tissues, we transferred GTPCH into aortic rings from BBd and Zucker diabetic fatty (ZDF) ra

112 In thoracic aortic rings from control rats, acetylcholine caused com

113 Our protocol can be applied to aortic rings from embryonic stage E18 through to adultho

114 ist-induced relaxation of eNOS-reconstituted aortic rings from eNOS knockout mice.

115 Aortic rings from HO-1(-/-) mice were unable to form cap

116 Finally, aortic rings from homozygous FHL2-null mice display abno

117 Aortic rings from IGFBP-1-overexpressing mice were hypoc

118 P and acetylcholine (ACh) vasorelaxations in aortic rings from normal and atherosclerotic rabbits in

119 In ex vivo experiments, exposure of isolated aortic rings from rats to H2O2 for 6 hours dramatically

120 Aortic rings from rats were incubated in serum-free medi

121 Disrupted angiogenesis in aortic rings from VimKO mice and in endothelial 3D sprou

122 An examination of aortic rings from wild-type mice and mice with homozygou

123 cysteine, HCl (BEC) produced vasodilation in aortic rings from young (Y) adult rats (maximum effect,

124 De-endothelialized Pkd2(+/-) aortic rings generated a higher maximum force (F(max)) t

125 Freshly cut aortic rings generated microvascular outgrowths in serum

126 METHODS AND Thoracic aortic rings harvested from transgenic reporter mice con

127 itionally, we demonstrate that NAADP dilates aortic rings in an endothelium- and NO-dependent manner.

128 al cells and stimulated the sprouting of rat aortic rings in culture.

129 e in tension of phenylephrine preconstricted aortic rings in response to the NO synthase inhibitor N(

130 in II failed to vasoconstrict 12/15-LOX(-/-) aortic rings in the absence of L-nitroarginine-methyl es

131 otes vascular relaxation based on studies of aortic rings in vitro.

132 served in beta(3)-null endothelial cells and aortic rings in vitro.

133 e (BNP) half-maximally relaxed precontracted aortic rings in wild-type mice at about 24 nM, but faile

134 ectivity was similar to that observed in rat aortic rings, in which 1400W was greater than 1000-fold

135 iogenesis in a subcutaneous in vivo assay of aortic ring-induced angiogenesis, but stimulated develop

136 Functional responses were unaffected in aortic rings isolated from 11betaHSD1(-/-) mice.

137 n or phenylephrine-dependent constriction in aortic rings isolated from 12/15-LOX(-/-) mice.

138 Comparable relaxations of aortic rings isolated from control and estrogen receptor

139 timulated release of EDNO were determined in aortic rings isolated from female and male wild-type and

140 ed vascular sprouting from Matrigel-embedded aortic rings isolated from uPA knock-out (uPA(-/-)) mice

141 radiol-induced vasorelaxation in depolarized aortic rings, isolated from male and female rats and mal

142 nd mannitol solutions had no vasoactivity in aortic rings, isotonic glucose produced a selective, ins

143 In isolated aortic rings, LXR activation of NOS caused relaxation, w

144 bcutaneous Matrigel injection and ex vivo in aortic ring Matrigel cultures.

145 tions, inhibited angiogenesis in an in vitro aortic ring model and in vivo in polyurethane sponges im

146 In an ex vivo rat aortic ring model of angiogenesis that includes cocultur

147 e formation of vascular sprouting in the rat aortic ring model of angiogenesis; and interferes with t

148 ectly induce vessel sprouting in the ex vivo aortic ring model, as well as endothelial cell prolifera

149 In aortic rings of C57BL/6 mice, bradykinin induced B2R-dep

150 migratory activity of endothelial cells from aortic rings of selected strains correlated with the in

151 Aortic rings of the baseline and hyperlipemic groups ela

152 angiogenic effect of TNFalpha in cultures of aortic rings or isolated endothelial cells, but stimulat

153 drove P(i)-stimulated calcification of mouse aortic ring organ cultures, which was suppressed by the

154 s reduced in SRF(SMKO) compared with control aortic rings owing to impairment of the NO pathway.

155 X) treatment (2.5 micrograms/ml for 4 hr) of aortic rings partially inhibited phenylephrine (PHE)-sti

156 Functional analysis of aortic ring preparations revealed improved endothelial f

157 in the aorta as well as vascular function of aortic ring preparations was assessed.

158 is expressed in arterial endothelial cells, aortic ring preparations were analyzed to determine whet

159 ts in each group had blood samples drawn and aortic rings removed to study vascular reactivity.

160 Ex vivo experiments with mouse aortic rings revealed a role for c-Met signaling in HGF-

161 after beta-methyl-cyclodextrin treatment of aortic rings reveals a concentration-dependent depletion

162 endocytosis of radioiodinated albumin using aortic ring segments from wild-type and Cav-1-null mice.

163 ylcholine (ACh) in phenylephrine-contracted, aortic ring segments was impaired by cholesterol feeding

164 c oxide (( *)NO)-dependent vasorelaxation of aortic ring segments was severely impaired in SCD mice,

165 Preincubation of rat aortic ring segments with Cl-L-Arg resulted in concentra

166 bited the capillary sprouting of EC from rat aortic ring segments.

167 These compounds relax pre-constricted rat aortic rings similar to known HNO donors.

168 ll migration and adhesion, tubule formation, aortic ring sprouting, and angiogenesis.

169 d endothelial cell proliferation and ex vivo aortic ring sprouting.

170 nsection (no-tension; n=15), resection of an aortic ring (tension; n=14) or resection and topical VEG

171 endothelium-dependent relaxation in isolated aortic rings that was superoxide dismutase inhibitable.

172 n, functional assays using EMP-treated mouse aortic rings that were performed under homeostatic condi

173 his model system, we now show that explanted aortic ring tissue and Matrigel implants from the smooth

174 also exhibited dose-dependent activity in an aortic ring tissue model of angiogenesis highlighting th

175 ter 15 weeks, but not 7 weeks, relaxation of aortic rings to acetylcholine was selectively impaired b

176 of aortic tissue, vasorelaxation response of aortic rings to exogenous ONOO-, No regeneration from ON

177 Exposure of rat aortic rings to lipopolysaccharide in vitro decreased th

178 ased the sensitivity (decreased the EC50) of aortic rings to phenylephrine (p < 0.0005), as did neona

179 g by measuring the physiological response of aortic rings to various stimuli.

180 Aortic rings treated for 30-60 min with extracellular Ca

181 that gp91ds-tat decreased O(2)(-) levels in aortic rings treated with Ang II (10 pmol/L) but had no

182 without endothelium and in intact male mouse aortic rings treated with NG-nitro-L-arginine, 17 beta-e

183 In rodent aortic rings, treatment with thrombospondin-1 increased

184 gration, tube formation, cell sprouting from aortic rings, tumor growth, and angiogenesis are all sig

185 blood cells (RBCs) to dilate preconstricted aortic rings under various O2 tensions.

186 However, IL6-stimulated aortic ring vessel sprouts had defective pericyte covera

187 n from macrophages and reduced the number of aortic ring vessel sprouts.

188 The reduction of NBT in intact aortic rings was 30+/-2 pmol x min(-1) x mg(-1) and was

189 ontaneous angiogenic response of freshly cut aortic rings was inhibited by 70% with a neutralizing an

190 d MIP-2), and ex vivo vascular reactivity in aortic rings were also measured.

191 Aortic rings were excised and isometric force responses

192 Rabbits were killed, and fresh aortic rings were harvested and maintained in oxygenated

193 Vascular reactivity of thoracic aortic rings were measured in organ chambers.

194 independent relaxation of preconstricted rat aortic rings, which was unaffected by L(G)-nitro-l-argin

195 in potent vasorelaxation in normal isolated aortic rings, which were impaired in atherosclerotic ver

196 Culture of aortic rings with antibody to major histocompatibility c

197 Treatment of quiescent aortic rings with exogenous VEGF stimulated angiogenesis

198 Preincubation of rat aortic rings with OxLDL resulted in an increase in argin

199 on, we also tested whether incubation of the aortic rings with PJ34 (3 micromol/L) or a variety of ot

200 In both male and female rat aortic rings without endothelium and in intact male mous