ライフサイエンスコーパス: neovessel

1 smooth muscle cell to support the developing neovessel.

2 ial or smooth muscle cells that comprise the neovessel.

3 peptide known to home specifically to tumor neovessels.

4 al drivers of angiogenesis in murine corneal neovessels.

5 incorporate into a subset of sprouting tumor neovessels.

6 ast-enhanced imaging that relies on perfused neovessels.

7 EGF-A) levels and expansion of Tie2-positive neovessels.

8 or endothelia and by recruiting pericytes to neovessels.

9 d apoptosis of tumor cells surrounding these neovessels.

10 P in the single layer of cells that line the neovessels.

11 e mRNA species in nucleated cells lining the neovessels.

12 rming a mural cell coat, stabilizing infarct neovessels.

13 nd-homing peptide that recognises angiogenic neovessels.

14 more specifically, in pathological sprouting neovessels.

15 to control EC proliferation in extra-retinal neovessels.

16 pathy (OIR) with pathologic proliferation of neovessels.

17 odels, and human surgical samples of retinal neovessels.

18 ze in the retina, particularly to pathologic neovessels.

19 F (PDGF-BB) is needed later to stabilize the neovessels.

20 vidence of traction to achieve regression of neovessels.

21 tinopathies is the formation of pathological neovessels.

22 een preformed channels and formed perfusable neovessels.

23 tiation (CD)-11b(+) macrophages and CD-31(+) neovessels.

24 y which DM induced LPA resistance of retinal neovessels.

25 ty measured as the total length of sprouting neovessels (12.63+/-3.66 mm in Ad-SM22-4A1-transduced ve

26 Moreover, in the mature scar, infarct neovessels acquire a mural cell coat that contributes to

27 ributes to the assembly and remodeling of BM neovessels after myelosuppression.

28 capture microdissection (LCM) to isolate the neovessels after OIR, we found decreased expression of C

29 he complement inhibitor Cd55 specifically on neovessels, allowing for their targeted removal while le

30 noted the emergence of CD31-negative patent neovessels and a concomitant loss of tumor homing of the

31 dothelial growth factor (VEGF) expression in neovessels and by attracting vessel-associated pericytes

32 ed SMC migration and recruitment of MCs into neovessels and elucidate the molecular signaling pathway

33 e myofibroblasts, which, in interaction with neovessels and HSC-MFs that mainly arise through differe

34 cylglycerols were found in areas surrounding neovessels and lacking either form of cholesterol.

35 , heterogeneous vessel population containing neovessels and mature vessels in advanced RB disease.

36 mens to evaluate the spatial distribution of neovessels and mature vessels.

37 ation of a mural cell coat investing infarct neovessels and protecting from dilative remodeling.

38 led to robust growth of blood and lymphatic neovessels and rapid allograft rejection after corneal p

39 signaling reduces NG2(+) MC recruitment into neovessels and subsequently reduces neovessel life span.

40 H phage) that distinguished between abnormal neovessels and the normal vasculature.

41 tead, recipient-derived stromal fibroblasts, neovessels, and infiltrating leukocytes were heavily rep

42 gioarchitecture and dysfunctionality of VEGF neovessels, and they identify a rational pharmacologic s

43 dministration in vivo markedly improved VEGF neovessel architecture and reduced neovascular leak.

44 pport the maintenance and stability of tumor neovessels are not well defined.

45 However, neovessels are susceptible for intraplaque hemorrhage, p

46 gnaling pathways contributing to these leaky neovessels are unclear.

47 sels, the factors that stabilize and pattern neovessels are undefined.

48 olds instead of developing into cells of the neovessel, as traditionally thought.

49 or of VEGF- and bFGF-induced CXCR4-dependent neovessel assembly in vivo and show that angiogenic effe

50 Finally, SH phage decorated abnormal neovessels at an early stage of their genesis.

51 Interestingly, tumor neovessels become leaky after maspin treatment, whereas

52 We demonstrate that neovessels become refractory to VEGF-A deprivation over

53 ate that angiogenic outgrowth, invasion, and neovessel branching increase with matrix cross-linking.

54 In its severest form, choroidal neovessels breach the macular Bruch's membrane, an extra

55 ed by immunohistochemistry to quantify blood neovessels (BVs) and lymphatic neovessels (LVs) to 3 wee

56 Vascular pruning, the removal of aberrant neovessels by apoptosis, is a vital step in this process

57 eases the interaction of leukemic cells with neovessels by down-regulating the expression of the adhe

58 induced regression of unstable nascent tumor neovessels by rapidly disrupting the molecular engagemen

59 ypoxia (pimonidazole), macrophages (RAM-11), neovessels (CD31), and hypoxia-inducible factor-1alpha w

60 ternative complement pathway in facilitating neovessel clearance by down-regulating the complement in

61 D0325901 promoted the formation of alphaSMA+ neovessels compared with PC only.

62 Abnormal neovessels consisted of at least three cell types that w

63 Intimal neovessels consistently immunostained for ET-1.

64 g studies suggest the possibility that these neovessels constitute dual-origin hybrids.

65 sions, unesterified cholesterol dominated in neovessel-containing areas enriched in glycophorin A.

66 ral macrophage density (r=0.79, P=0.007) and neovessel counts (r=0.87, P=0.001) on immunohistochemist

67 D45(+) cells generated endothelial cells and neovessels de novo in a hindlimb model of ischaemia and

68 to low oxygen, mimicking a characteristic of neovessels, decreased the expression of the complement i

69 Neovessel density at 28 days was also reduced (23+/-42 v

70 ls decreased xenograft growth and suppressed neovessel density, suggesting a role for endogenous H2S

71 A neovessel-derived signal mediated by prostacyclin trigge

72 In addition to increasing the contrast of neovessels detected at baseline, alpha(v)beta(3)-GNBs al

73 e- and strain-matched control mice to assess neovessel development and regression in an oxygen-induce

74 mechanically ideal substratum for promoting neovessel development.

75 This may prevent thrombosis of neovessels during angiogenesis but renders hemophiliacs

76 An alternate proposal suggests that neovessels form from endothelial progenitors able to ass

77 use airways showed a significant decrease in neovessel formation and endothelial cell proliferation i

78 A variety of factors cooperate to regulate neovessel formation and persistence.

79 that macrophage infiltration is critical for neovessel formation and provides a strategy for predicti

80 In these diseases, the balance between neovessel formation and regression determines blindness,

81 genic growth factors in transplanted hearts, neovessel formation appears scant.

82 thway to curtail the effects of CTGF/CCN2 on neovessel formation associated with ischemic retinopathy

83 Noninvasive methods for characterizing neovessel formation during angiogenesis are currently la

84 n mediate aspects of vascular remodeling and neovessel formation during atherogenesis and other chron

85 tic mice had reduced blood flow recovery and neovessel formation in a hindlimb ischemia model compare

86 l implications for the therapy of pathologic neovessel formation in the retina of patients with PDR.

87 Macrophages are a critical driver of neovessel formation in tissue-engineered vascular grafts

88 xpression also restores PT-ECFC capacity for neovessel formation in vivo.

89 on of PDGFRbeta(+) cell proliferation before neovessel formation is sufficient to inhibit scaffold fo

90 errantly, in the subsequent ischemia-induced neovessel formation phase of ROP.

91 rganotypic model of angiogenic sprouting and neovessel formation that originates from preformed artif

92 lial GF (VEGF) is required early to initiate neovessel formation while platelet-derived GF (PDGF-BB)

93 To identify proteinases critical to neovessel formation, an ex vivo model of angiogenesis ha

94 By contrast, neovessel formation, in vitro and in vivo, is dependent

95 at are characterized by aberrant increase in neovessel formation, including cancer.

96 neutralization of IL-6 significantly reduced neovessel formation.

97 uited to neoangiogenic niches and to support neovessel formation.

98 dothelial precursors that may participate in neovessel formation.

99 re it plays an indispensable role in driving neovessel formation.

100 ytic activity, endothelial cell invasion, or neovessel formation.

101 ts and evaluated the role of cell seeding on neovessel formation.

102 nalogous mouse models to study mechanisms of neovessel formation.

103 s of these diseases is angiogenesis (AG) and neovessel formation.

104 hereas they persisted in the areas that were neovessel-free.

105 of endothelial tube formation, sprouting of neovessels from murine aorta, and angiogenesis in Matrig

106 ularization, we discovered that pathological neovessels generate extraordinarily high voltage.

107 enduring vascular response, IGF-1 stabilized neovessels generated from primary endothelial cells deri

108 Pathological neovessels growing into the normally avascular photorece

109 ovel therapeutic strategy by both suppressed neovessel growth and curtailing fibrosis typically assoc

110 ne of the main consequences of inhibition of neovessel growth and vessel pruning produced by angiogen

111 termines blindness, making the modulation of neovessel growth highly desirable.

112 Neovessel growth, density, and length were graded at int

113 hich recapitulates ischemia-induced aberrant neovessel growth, is characterized by increased expressi

114 at intervals using a semiquantitative visual neovessel growth-rating scheme (angiogenic index, 0-16 s

115 ured in an environment that does not lead to neovessel growth.

116 Clearance of senescent cells suppressed neovessel growth.

117 apid regression of specific subsets of tumor neovessels has opened up new avenues of research to iden

118 The neovessels in alpha(M)(-/-) mice were leaky and immature

119 was localized to fibrous cap SMA+ cells and neovessels in plaques.

120 y immunohistochemistry to the endothelium of neovessels in rat tissues undergoing angiogenesis during

121 e secreted angiostatin specifically targeted neovessels in the brain tumors, as evidenced by the dimi

122 quently occurred around thin-walled, dilated neovessels in the infarct border zone and was accompanie

123 poietin-1, a cytokine that "normalizes" VEGF neovessels in vivo, activated Rac1 and improved cord for

124 ic growth factors in the formation of mature neovessels in vivo.

125 s, and its level of expression is reduced in neovessels in vivo.

126 of excess opticin inhibited the formation of neovessels in wild-type mice.

127 at form fibrotic septa, preferentially along neovessels, in murine and human liver disorders, irrespe

128 ctively induces regression of unstable tumor neovessels, in part through disruption of VE-cadherin si

129 Our data suggest that sensory nerves and neovessels inhibit each other in the cornea.

130 al cell migration in vitro and the growth of neovessels into subcutaneous implants of Matrigel in viv

131 hase of OIR, prevented formation of aberrant neovessels into the vitreous by suppressing proliferatio

132 )) scaffold is formed before infiltration of neovessels into this scaffold to form CNV lesions, and t

133 atment resulted in significant regression of neovessel invasion area (P < 0.05).

134 luding neovascular area, vessel caliber, and neovessel invasion area.

135 Abnormal development of neovessels is associated with early expression of distin

136 Moreover, timely regeneration of BM neovessels is essential for reconstitution of hematopoie

137 While DM had no effect on the formation of neovessels, it prevented LPA-induced regression.

138 Active modulation of these tumor neovessels lead to distinct changes in tumor vascular pe

139 ent into neovessels and subsequently reduces neovessel life span.

140 ral corneal epithelium, leakiness of corneal neovessels, loss of axons in corneal stroma, and loss of

141 uantify blood neovessels (BVs) and lymphatic neovessels (LVs) to 3 weeks after implantation.

142 ay also impair TGFbeta signaling and hypoxic neovessel maturation.

143 ecruitment and smooth muscle coverage in the neovessels of the border zone of infarcted myocardium ar

144 e detected donor-derived CEPs throughout the neovessels of tumors and Matrigel-plugs in an Id1+/-Id3-

145 uiescent and unable to spontaneously produce neovessels, only VEGF was capable of inducing an angioge

146 , 5 and 2 cases), 5 scaffolds showed intimal neovessels or marked peristrut low-intensity areas.

147 igration, basement membrane degradation, and neovessel organization.

148 sion of CTGF/CCN2 harnessed ischemia-induced neovessel outgrowth in oxygen-induced retinopathy mice.

149 d to express CCN1 harnessed ischemia-induced neovessel outgrowth without adversely affecting the phys

150 glioma development and the quantification of neovessels over time.

151 a nonsignificant decrease in the density of neovessels (P = 0.94).

152 mounts and identified an increased number of neovessels, peaking at postnatal day 17 (P17; P=0.001).

153 Endogenous VEGF signalling prevents excess neovessel pericyte coverage, and is required for VSMC re

154 ever, VEGF induced the formation of immature neovessels, providing an explanation for its lesser effi

155 could be therapeutically adapted for driving neovessel regression in ocular diseases.

156 so involved in recruitment of mural cells by neovessels, regulating maturation of the infarct vascula

157 As expected, the recognition of abnormal neovessels relied on the unique peptide insert of SH pha

158 a few millimeters without the recruitment of neovessels since cancer cells require access to blood ve

159 this end, we used an ex vivo assay in which neovessels sprouted from retinal explants (isolated from

160 Furthermore, Slit3 stimulates neovessel sprouting ex vivo and new blood vessel growth

161 and Akt, but not p38 MAPK, are necessary for neovessel sprouting.

162 , but significantly potentiated VEGF-induced neovessel sprouting.

163 trix-degrading proteases as well as immature neovessels sprouting into the lesion.

164 ol of lumen and tube formation and, finally, neovessel stability and maturation.

165 tomes not only induce AG/WH but also promote neovessel stabilization and endothelial cell survival fo

166 liferating bile ductules and its presence on neovessels suggests that Notch signaling may be importan

167 HCMV secretome to preformed vessels extended neovessel survival, but this effect was blocked by neutr

168 le gene delivery of VEGF results in immature neovessels that ultimately regress.

169 wn about the factors that drive sprouting of neovessels, the factors that stabilize and pattern neove

170 on or from pericytes that are present in the neovessels themselves.

171 mAbs to VE-cadherin by blocking assembly of neovessels, thereby inhibiting tumor growth.

172 in astrocytes and reprogrammed pathological neovessels to a physiological phenotype, hastening vascu

173 us (DM) influences responsiveness of retinal neovessels to lysophosphatidic acid (LPA) and to elucida

174 The sensitivity of growing neovessels to these stimuli was adjusted so that AngioFE

175 were to evaluate the spatial distribution of neovessels versus mature vessels in both human retinobla

176 ings suggest TEVGs transform into functional neovessels via an inflammatory process of vascular remod

177 6 inhibited retinal vascular lesion area and neovessel volume in a laser-induced choroidal neovascula

178 As a consequence, the resulting neovessel was entirely of host cell origin.

179 Integrity of suture-induced corneal neovessels was assessed with high molecular weight dextr

180 In human RB, the percentage of neovessels was higher in the periphery of the tumor than

181 The percentage of large-caliber neovessels was higher in the periphery than in the cente

182 atients, and the presence of macrophages and neovessels was quantified by immunohistochemistry.

183 ntiate into the mature vascular cells of the neovessel, we implanted an immunodeficient mouse recipie

184 Immunohistochemical analysis showed that the neovessels were composed of human and mouse endothelial

185 Intraplaque neovessels were found predominantly in macrophage-rich h

186 distribution of large-caliber vessels (i.e., neovessels were higher in the periphery for large [P = 0

187 ively), whereas CE grade and the presence of neovessels were not.

188 Indeed, IGF-1 lost its ability to stabilize neovessels when the Erk pathway was inhibited pharmacolo

189 In contrast to VEGF, IGF-1 stabilizes neovessels, which is dependent on Erk activity and assoc

190 ited the expression of S1P(1) polypeptide on neovessels while concomitantly suppressing vascular stab

191 embly and induce regression of nascent tumor neovessels, with minimal toxicity and without affecting

192 colocalization of asTF with macrophages and neovessels within complicated, but not uncomplicated, hu

193 There were many neovessels within the intima of CAV lesions.

194 Neovessels within the matrigel stained positive for alph

195 The presence of patent neovessels within vascular occlusions in chronic thrombo