ライフサイエンスコーパス: vasa vasorum

1 use ECs line the vascular epithelium and the vasa vasorum.

2 from the development of immature neointimal vasa vasorum.

3 complete tissue integration and formation of vasa vasorum.

4 osclerotic plaque and associated adventitial vasa vasorum.

5 s the proliferation and intimal extension of vasa vasorum.

6 ural changes, including the formation of new vasa vasorum.

7 ssels, with proportionally more second-order vasa vasorum.

8 etween VEGF/VPF immunostaining and extent of vasa vasorum.

9 espectively, P < 0.01) and in the density of vasa vasorum (1.84+/-0.05/mm2 vs. 4.73+/-0.24/mm2; respe

10 ro-computed tomography techniques that image vasa vasorum anatomy in relation to the atheroma.

11 ed especially by an increase of second-order vasa vasorum and disorientation of normal vasa vasorum s

12 ansplanted islets received blood supply from vasa vasorum and had access to drainage through venous t

13 We observed more extensive vasa vasorum and intimal neovascularization in knockout

14 cytes and T lymphocytes, and the role of the vasa vasorum and surrounding perivascular adipose tissue

15 IP NCs arose directly from adventitial vasa vasorum and were anatomically and quantitatively re

16 f helping detect and even grade intracranial vasa vasorum, and this may provide new insights into our

17 nd with the development of vascular disease, vasa vasorum are known to develop.

18 Macrophages in the plaque and around vasa vasorum are reduced, but we detect no direct effect

19 onstrate that rPAI-1(23) treatment decreased vasa vasorum area and length, which was supported by mic

20 hat the coronary vessel wall, especially the vasa vasorum, as well as bone marrow-derived endothelial

21 In conclusion, rPAI-1(23) inhibits growth of vasa vasorum, as well as vessels within the adjacent pla

22 dventitia, particularly within microvessels (vasa vasorum) but not in cells of the intima or media.

23 rPAI-1(23)-stimulated mechanisms that cause vasa vasorum collapse.

24 reconstructed confocal microscopy images of vasa vasorum demonstrate that rPAI-1(23) treatment decre

25 We observe vasa vasorum density correlates highly with the extent o

26 prevents the increase in VEGF expression and vasa vasorum density of coronary arteries in experimenta

27 Vasa vasorum density was higher in the HC group compared

28 lloon-injured coronary arteries, adventitial vasa vasorum density was increased (3.16+/-0.17/mm2 vs.

29 nned, and reconstructed, and quantitation of vasa vasorum density was performed.

30 Plaque size and vasa vasorum density were compared to 2 controls: mice f

31 from the artery lumen and outer adventitial vasa vasorum, deposit proatherogenic plasma molecules, r

32 a and disarray, and stenotic arteries in the vasa vasorum due to medial SMC proliferation.

33 ccount for the relative lack of intracranial vasa vasorum early in life.

34 culture adventitial fibroblasts (AdvFBs) and vasa vasorum endothelial cells (VVECs) from the adventit

35 ic cells and macrophages), progenitor cells, vasa vasorum endothelial cells and pericytes, and adrene

36 ctivity was found in luminal and adventitial vasa vasorum endothelium.

37 To inhibit growth of vasa vasorum in atherogenic mice and assess its effect o

38 Recent attention has focused on the role of vasa vasorum in atherosclerotic and restenotic coronary

39 The three-dimensional anatomy of the vasa vasorum in early coronary atherosclerosis is unknow

40 causes regression or collapse of adventitial vasa vasorum in hypercholesterolemic mice by stimulating

41 titate three-dimensional spatial patterns of vasa vasorum in normal and balloon injured porcine coron

42 ate the three-dimensional spatial pattern of vasa vasorum in normal and experimental hypercholesterol

43 ssessment of the therapeutic response of the vasa vasorum in patients with atherosclerotic plaque.

44 origin of plaque vasculature and the role of vasa vasorum in plaque growth.

45 We also studied the spatial growth of vasa vasorum in regions of neointimal formation.

46 Coronary arteries contain a network of vasa vasorum in the adventitia.

47 iew offers insight into the possible role of vasa vasorum in the development of intracranial vascular

48 These data demonstrate that formation of new vasa vasorum in vasculitis is regulated by inflammatory

49 arteries suggests that the formation of new vasa vasorum is determined by the nature of the immune r

50 ionally, neovascularization arising from the vasa vasorum may promote atherosclerotic plaque progress

51 es is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica m

52 mplex layer of the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune c

53 mplex layer of the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune c

54 al nitric oxide synthase (due to ingrowth of vasa vasorum), neointima formation, and loss of smooth m

55 pport a role for the endogenous ET system in vasa vasorum neovascularization in early coronary athero

56 in (ET) receptor antagonism reduces coronary vasa vasorum neovascularization in experimental hypercho

57 , a promoter of adventitial inflammation and vasa vasorum neovascularization in experimental models o

58 hanistic role of the endogenous ET system in vasa vasorum neovascularization in hypercholesterolemia

59 Cs, in a process involving ET-1, to regulate vasa vasorum neovascularization occurring in the adventi

60 ed phases, the role of eccentric remodeling, vasa vasorum neovascularization, and mechanisms of plaqu

61 molecular mechanisms regulating adventitial vasa vasorum neovascularization, which occurs in the pul

62 ede "macrovascular endothelial dysfunction." Vasa vasorum neovascularization, with endothelial leakag

63 increased, suggesting a mechanistic role for vasa vasorum neovascularization.

64 n the coronary arterial wall as well as with vasa vasorum neovascularization.

65 gests that adventitial neovascularization of vasa vasorum occurs in experimental hypercholesterolemic

66 Normal vasa vasorum originated from the coronary artery lumen,

67 ix can be imaged, as can angiogenesis of the vasa vasorum, plaque inflammation, and fibrin deposits o

68 growth factor-2 as mediators associated with vasa vasorum proliferation.

69 es of vasa vasorum were defined: first-order vasa vasorum ran longitudinally parallel to the vessel a

70 on," which is composed of dysfunction of the vasa vasorum's endothelium as well as "microcellular end

71 CML was localized to aortic and aortic vasa vasorum smooth muscle but not to collagen or elasti

72 er vasa vasorum and disorientation of normal vasa vasorum spatial pattern.

73 After 12 weeks, coronary vasa vasorum structure was assessed by three-dimensional

74 the quantitative response of the adventitial vasa vasorum to balloon-induced coronary injury.

75 -vessel vasculitis affecting branches of the vasa vasorum tree.

76 to neovascularization in the coronary artery vasa vasorum (VV).

77 The density of newly formed vasa vasorum was proportional to vessel stenosis (r = 0.

78 ntiangiogenic effect of TSP-1, the number of vasa vasorum was reduced in aortas from diabetic rats.

79 Two different types of vasa vasorum were defined: first-order vasa vasorum ran

80 In normal arteries, vasa vasorum were restricted to the adventitia, but in i

81 lammation; and to stimulate expansion of the vasa vasorum, which can act as a conduit for continued i

82 to support development and maturation of the vasa vasorum within varying plaque types.