ライフサイエンスコーパス: aortic ring

1 ased protein glutathiolation in isolated rat aortic rings.

2 ion produced significant force generation in aortic rings.

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

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

5 neous angiogenic response of freshly cut rat aortic rings.

6 ormance, and impaired vascular relaxation of aortic rings.

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

8 endothelium-dependent relaxant responses of aortic rings.

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

10 e-precontracted endothelium-denuded thoracic aortic rings.

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

12 constriction in isolated endothelium-denuded aortic rings.

13 n isolated rat pulmonary artery and thoracic aortic rings.

14 r kallikrein, induced vascular relaxation of aortic rings.

15 oth muscle cells (HVSMCs) and isolated mouse aortic rings.

16 onduit and resistance vasculature by ex vivo aortic rings.

17 es and producing vasorelaxing effects on rat aortic rings.

18 GABA had no relaxing effect on rat aortic rings.

19 essed using norepinephrine precontracted rat aortic rings.

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

21 production and vessel relaxation in isolated aortic rings.

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

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

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

25 In isolated aortic rings, ACh-mediated relaxation was impaired follo

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

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

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

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

30 bilical vein endothelial cells (HUVECs), rat aortic ring and mouse cornea were used to detect the ang

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

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

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

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

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

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

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

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

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

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

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

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

43 t vasorelaxation induced by acetylcholine in aortic rings and reduced NADPH oxidase activity in DOCA-

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

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

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

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

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

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

50 dependently enhanced calcification in murine aortic rings, and extravasated CD235a-positive erythrocy

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

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

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

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

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

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

57 The aortic ring assay allows analysis of cellular proliferat

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

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

60 uced potency to promote calcification in the aortic ring assay and after injection into murine vascul

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

62 Similarly, the aortic ring assay and CAM assay showed that PSP-2 evokes

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

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

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

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

67 -13 inhibited capillary sprouting in the rat aortic ring assay and vessel growth in the Matrigel plug

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

69 The aortic ring assay demonstrated that new vessels were pro

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

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

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

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

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

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

76 outing was assessed by the chicken and sheep aortic ring assay, and vascular pattern formation was st

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

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

79 Using the ex vivo aortic ring assay, we set out to dissect the interaction

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

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

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

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

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

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

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

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

88 Aortic ring assays reveal induced AnxA1 expression on sp

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

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

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

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

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

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

95 itro competition binding assays, ex vivo rat aortic ring bioassays and BRET-based biosensor experimen

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

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

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

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

100 fication assays, ex vivo by using the murine aortic ring calcification model, and in vivo after murin

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

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

103 Abdominal aortic ring contraction experiments revealed that PGF2al

104 ddition, VSMC stiffness (-46.6%) and ex vivo aortic ring contraction force (-40.1%) were lowered and

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

106 17 beta-Estradiol-induced relaxation of rat aortic rings could not be prevented by cycloheximide or

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

108 ry mouse and human VSMCs, as well as ex vivo aortic ring cultures, we demonstrated that treatment wit

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

110 a murine model impaired endothelium-mediated aortic ring dilation, which was then reversed by 3-week

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

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

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

114 Exposure of the aortic rings embedded in 3D fibrillar collagen to recomb

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

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

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

118 ls and attenuated ANP-mediated relaxation of aortic rings ex vivo.

119 4 activation and impaired SMC outgrowth from aortic rings ex vivo.

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

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

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

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

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

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

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

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

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

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

130 on (from 0.1 nM to 100 uM) were performed on aortic rings from diabetic and non-diabetic rats after a

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

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

133 Furthermore, ex vivo aortic rings from GDF10(-/-) mice exhibited increased HA

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

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

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

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

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

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

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

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

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

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

144 Freshly cut aortic rings generated microvascular outgrowths in serum

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

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

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

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

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

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

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

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

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

154 cg1 deficiency increased vasoconstriction in aortic rings induced by the alpha(1)-AR agonist phenylep

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

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

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

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

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

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

161 ulmonary microvascular endothelial cells and aortic rings isolated from wild-type, endothelium-specif

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

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

164 more profound stress relaxation than did the aortic ring itself.

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

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

167 g microvessel formation in an ex vivo rabbit aortic ring model and by inhibiting endothelial cell exp

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

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

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

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

172 dependently of cereblon in the ex vivo mouse aortic ring model.

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

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

175 Aortic rings of the baseline and hyperlipemic groups ela

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

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

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

179 bserved in endothelial cells ( P<0.0001) and aortic rings ( P=0.0060) from End.LepR-KO mice, and muri

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

181 Functional analysis of aortic ring preparations revealed improved endothelial f

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

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

184 on in mgs; aortic ring -PVAT = 4578 +/- 190; aortic ring + PVAT = 2730 +/- 274, p < 0.05).

185 no benefit in cumulative stress relaxation (aortic ring +/- PVAT = 4122 +/- 176; p > 0.05 vs -PVAT).

186 of stress relaxation (final tension in mgs; aortic ring -PVAT = 4578 +/- 190; aortic ring + PVAT = 2

187 cacy in H(2)S-mediated relaxation in ex vivo aortic ring relaxation models.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 Notably, chronic exposure of aortic rings to endorepellin for 7-9 days markedly suppr

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

207 rtic prostacyclin production, the ability of aortic rings to inhibit platelet aggregation and plasma

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

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

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

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

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

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

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

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

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

217 Aortic rings underwent functional evaluation, histology,

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

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

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

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

222 la-(1-5) effects on cardiomyocytes and mouse aortic rings were abolished only by MrgD genetic deletio

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

224 Aortic rings were excised and isometric force responses

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

226 Murine aortic rings were incubated in NG or HG for 24 h.

227 Aortic rings were incubated with citrullinated histone H

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

229 Following incubation, the aortic rings were placed in an organ chamber bath contai

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

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

232 Culture of aortic rings with antibody to major histocompatibility c

233 Treatment of quiescent aortic rings with exogenous VEGF stimulated angiogenesis

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

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

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