ライフサイエンスコーパス: reendothelialization

1 wild-type mice has no effect, apoE4 impairs reendothelialization.

2 whether estrogen was capable of accelerating reendothelialization.

3 eading to stent malapposition and incomplete reendothelialization.

4 oxide synthase and repressed carotid artery reendothelialization.

5 e impaired in diabetes, resulting in delayed reendothelialization.

6 apolipoprotein A-I expression rescues normal reendothelialization.

7 while accelerating, rather than inhibiting, reendothelialization.

8 arly growth response factor-1 (Egr-1) during reendothelialization.

9 in endothelial cells (ECs), thereby delaying reendothelialization.

10 nificant difference in the degree of luminal reendothelialization.

11 dothelial cell (EC) migration contributes to reendothelialization after angioplasty or rupture of ath

12 d whether statin therapy may also accelerate reendothelialization after carotid balloon injury.

13 t, in contrast to E2, it fails to accelerate reendothelialization after carotid electric injury.

14 Importantly, reendothelialization after focal carotid endothelial inj

15 ols with CRP of <1 microg/mL, carotid artery reendothelialization after perivascular electric injury

16 leling the in vitro findings, carotid artery reendothelialization after perivascular electric injury

17 Reendothelialization after VBT is not completed at 6 mon

18 ated MAPK pathways, possibly contributing to reendothelialization and angiogenesis after vascular inj

19 roliferation and migration are important for reendothelialization and angiogenesis.

20 Estradiol accelerates reendothelialization and attenuates medial thickening af

21 utoregulation in vascular ECs, L5 may impair reendothelialization and collateralization in diabetes.

22 In summary, decreased reendothelialization and enhanced endothelial apoptosis,

23 verexpression of endostatin led to decreased reendothelialization and increased apoptosis of luminal

24 VEGF overexpression accelerated reendothelialization and increased luminal endothelial c

25 ation of anti-TSP1 antibody could facilitate reendothelialization and inhibit neointimal thickening i

26 s repair of injured arteries by facilitating reendothelialization and inhibiting neointima developmen

27 d the effect of endostatin overexpression on reendothelialization and neointima formation in a mouse

28 blue staining) or 2 weeks for evaluation of reendothelialization and neointimal formation.

29 ting restenosis, while selectively promoting reendothelialization and preserving EC function.

30 insights and therapeutic targets to improve reendothelialization and reduce restenosis in diabetes.

31 elivery of antibody against TSP1 facilitated reendothelialization and reduced neointimal lesion forma

32 uced diabetic mice, 1,25-VitD3 also promoted reendothelialization and restored the impaired angiogene

33 and/or endogenous VEGF by VEGF-trap delayed reendothelialization and significantly increased neointi

34 er coronary interventions may reflect plaque reendothelialization and stabilization.

35 This lack of discrimination delays reendothelialization and vascular healing, increasing th

36 g in the labyrinth, failed SA remodeling and reendothelialization, and markedly reduced numbers of ma

37 Unexpectedly, reendothelialization (assessed by resistance to Evans bl

38 ed nonirradiated vessels, there was complete reendothelialization at 1 month, and platelet recruitmen

39 anning electron microscopy showed incomplete reendothelialization at 1 month, and these areas demonst

40 as well as stimulating a 2-fold increase in reendothelialization at 14 days after injury.

41 rap overexpression alone also led to delayed reendothelialization at 2 weeks (P<0.01) and increased n

42 ithout a significant change in the degree of reendothelialization at 2 weeks.

43 on at the time of balloon injury accelerated reendothelialization at 4 weeks compared with saline (P<

44 ble receptor molecule results in accelerated reendothelialization at sites of balloon angioplasty, su

45 mice to evaluate how cholesterol influences reendothelialization, atherosclerosis, and EPC function

46 ts not only induced faster and more complete reendothelialization, but also effectively improved neoi

47 We hypothesized that reendothelialization by cell therapy would modulate aort

48 marrow-derived EPC incorporation at sites of reendothelialization, carotid injury was established in

49 Tissue factor overexpression accelerated reendothelialization compared with controls at 2 weeks a

50 Delayed reendothelialization contributes to restenosis after ang

51 dostatin serum levels, whereas the degree of reendothelialization correlated negatively with endostat

52 Furthermore, poor reendothelialization correlated with increased neointima

53 ured arteries is associated with accelerated reendothelialization, enhanced endothelium-dependent vas

54 euthanatized after 1 week for evaluation of reendothelialization (Evans blue staining) or 2 weeks fo

55 ion of a neutralizing VEGF antibody impaired reendothelialization following balloon injury performed

56 leling the in vitro findings, carotid artery reendothelialization following perivascular electric inj

57 The effects of CO on reendothelialization have not been evaluated.

58 ol and EDC equally stimulated carotid artery reendothelialization in an ERalpha- and G protein-depend

59 ter injury disclosed significantly increased reendothelialization in arteries treated with C6.7 antib

60 damage and vascular dysfunction by improving reendothelialization in mice.

61 ber of angiogenic myeloid cells and promoted reendothelialization in the carotid artery injury model.

62 ID significantly enhanced reendothelialization in the injured carotid arteries as

63 Thus, CRP downregulates eNOS and attenuates reendothelialization in vivo in mice, and this action of

64 ell migration and proliferation in vitro and reendothelialization in vivo.

65 ic denudation of the endothelium accelerated reendothelialization in vivo.

66 cell proliferation, but that did not prevent reendothelialization in vivo.

67 Reendothelialization involves endothelial progenitor cel

68 The rate of reendothelialization is critical in neointima formation

69 Carotid artery reendothelialization is decreased in ApoER2(-/-) mice, a

70 Reendothelialization is impaired by malfunctioning EPCs

71 Furthermore, reendothelialization is impaired in SR-BI(-/-) mice.

72 the hypothesis that the EPC contribution to reendothelialization may be impaired in diabetes, result

73 esized that estrogen-induced acceleration of reendothelialization might be mediated in part by effect

74 y of proangiogenic miR-126 was tested in the reendothelialization model.

75 Relaxation and reendothelialization of carotid arteries and circulating

76 It has been suggested that reendothelialization of damaged blood vessels protects a

77 represent a promising cell source for rapid reendothelialization of damaged vasculature after expans

78 stradiol treatment significantly accelerated reendothelialization of injured arterial segments within

79 ilability in the carotid artery and improved reendothelialization of injured carotid arteries in vivo

80 t in 34 male Sprague-Dawley rats accelerated reendothelialization of the balloon-injured arterial seg

81 ion formation were related to the functional reendothelialization of the damaged vessel, endothelium-

82 d rat, at least in part, by facilitating the reendothelialization of the damaged vessel.

83 us air controls, and in vivo, it accelerates reendothelialization of the denuded artery by day 4 afte

84 n endothelial proliferation as determined by reendothelialization of the denuded rat aorta.

85 e-1, showed rapid and nearly complete (>90%) reendothelialization of the denuded vessels in the G-CSF

86 upts endothelial cell (EC) proliferation and reendothelialization of the injured vessel.

87 ssion of E2F1 at the site of injury improves reendothelialization of the injured vessel.

88 ll (EC) proliferation and negatively affects reendothelialization of the injured vessel.

89 elial precursors showed defective homing and reendothelialization of the retinal vasculature compared

90 ment in endothelium-dependent relaxation and reendothelialization of their injured carotid arteries.

91 In contrast, estradiol did not accelerate reendothelialization or augment EPC mobilization into th

92 eloping strategies aimed at accelerating the reendothelialization process.

93 imals exhibited reduced restenosis, complete reendothelialization, reduced hypercoagulability, and re

94 Delinquent reendothelialization (rET) has been shown to have a perm

95 ce, LXR activation stimulated carotid artery reendothelialization via LXRbeta- and ERalpha-dependent

96 ascular injury by promoting EPC function and reendothelialization via upregulation of heme oxygenase-

97 Acceleration of reendothelialization via VEGF-2 gene-eluting stents prov

98 lanted into nondiabetic mice, revealing that reendothelialization was impaired in the recipients of d

99 that was survived to 2 weeks (n=5), luminal reendothelialization was measured via CD-31 staining.

100 Reendothelialization was nearly complete in the VEGF ste

101 Reendothelialization was paralleled by a decrease in inf

102 Reendothelialization was significantly reduced in diabet

103 Delayed reendothelialization was suggested as a pivotal cause, b

104 levels and improvements of EPC function and reendothelialization were all abrogated by pharmacologic

105 nical consequence of these stents is delayed reendothelialization, which may increase the risk of lat

106 stradiol caused a dose-dependent increase in reendothelialization, which was measured as absolute are

107 The impaired reendothelialization with CRP was mimicked by NOS antago