ライフサイエンスコーパス: hyperpermeability

1 Rho signaling, monolayer disruption, and EC hyperpermeability.

2 lding domain (AP-Cav) reduces eNOS-regulated hyperpermeability.

3 ed attenuation of IL-1beta-induced monolayer hyperpermeability.

4 )-induced glomerular endothelial cell (GEnC) hyperpermeability.

5 s beneficial effects against TBI-induced BBB hyperpermeability.

6 mbin, concomitant with increased endothelial hyperpermeability.

7 time course correlating with that of venular hyperpermeability.

8 at FAK contributes to VEGF-elicited vascular hyperpermeability.

9 n but significantly attenuated VEGF-elicited hyperpermeability.

10 itrite (ONOO(-)), we abrogated B box-induced hyperpermeability.

11 suffer both systemic and pulmonary vascular hyperpermeability.

12 tor (VEGF)-induced angiogenesis and vascular hyperpermeability.

13 lial growth factor (VEGF)-localized vascular hyperpermeability.

14 rs of inflammation, coagulation and vascular hyperpermeability.

15 of histologic evidence of mucosal damage and hyperpermeability.

16 nger) on the development of cytokine-induced hyperpermeability.

17 liorate the development of IFN-gamma-induced hyperpermeability.

18 mediator of cytokine-induced gut epithelial hyperpermeability.

19 nhibition reduced SIN-1-but not SNAP-induced hyperpermeability.

20 e characterized by angiogenesis and vascular hyperpermeability.

21 e to several mediators that increase venular hyperpermeability.

22 have deleterious effects related to vascular hyperpermeability.

23 dal exudation by reducing choroidal vascular hyperpermeability.

24 of a distinct CNV corresponding to the ICGA hyperpermeability.

25 I) is characterized by increased endothelial hyperpermeability.

26 during sepsis and, therefore, contributes to hyperpermeability.

27 oform VEGF165 stimulates vascular growth and hyperpermeability.

28 endothelial junction disruption and vascular hyperpermeability.

29 n and p120 at the adherens junction and with hyperpermeability.

30 in the cytosol is necessary for PAF-induced hyperpermeability.

31 asma membrane to the cytosol is required for hyperpermeability.

32 the cytosol is necessary for agonist-induced hyperpermeability.

33 I and is not involved in endothelial barrier hyperpermeability.

34 ling increases inflammation-induced vascular hyperpermeability.

35 o deliver NO to subcellular targets to cause hyperpermeability.

36 angiogenesis and associated chronic vascular hyperpermeability.

37 naling in a mouse model for retinal vascular hyperpermeability.

38 esponsible for caveolae-mediated endothelial hyperpermeability.

39 s tumor growth and tumor-associated vascular hyperpermeability.

40 ase pathway determines endothelial cell (EC) hyperpermeability after injurious stimuli.

41 ed 1) VEGF signaling pathway leading to GEnC hyperpermeability and 2) the modulatory effects of stati

42 in regulating VVO function in acute vascular hyperpermeability and angiogenesis.

43 preconditioned with ESCs could reverse cell hyperpermeability and apoptosis in vitro and protect aga

44 ents IFN-gamma-induced intestinal epithelial hyperpermeability and ATP depletion, possibly by fosteri

45 rowth factor antagonist, blocks the vascular hyperpermeability and blood flow increases induced by el

46 y mediators of VEGF-induced endothelial cell hyperpermeability and demonstrates the modulatory effect

47 H(2)O(2)-induced pulmonary vascular albumin hyperpermeability and edema formation.

48 t mice were also refractory to lung vascular hyperpermeability and edema in a lipopolysaccharide-indu

49 Vascular hyperpermeability and excessive neovascularization are h

50 yte adhesion induced by endothelial junction hyperpermeability and ICAM-1 expression during inflammat

51 es (ROS) propagate blood-brain barrier (BBB) hyperpermeability and inflammation following TBI.

52 tic applications in conditions of intestinal hyperpermeability and inflammation.

53 sion and nitric oxide production to vascular hyperpermeability and intensified anaphylactic responses

54 in angiogenesis, and JAM-C blockade reduced hyperpermeability and neovascularization in hypoxia-indu

55 se VEGF 121 genes induced localized vascular hyperpermeability and produced PE only after direct impl

56 otective mechanism of ANP against pathologic hyperpermeability and suggests a novel pharmacological i

57 nd-binding domain of RAGE, reversed vascular hyperpermeability and suppressed accelerated atheroscler

58 of calpains in mediating BBB dysfunction and hyperpermeability and to test the effect of calpain inhi

59 nflammatory mediators that cause endothelial hyperpermeability and vascular leakage.

60 thermore, PGD(2) attenuated cytokine-induced hyperpermeability and zonula occludens-1 downregulation

61 LPS induced a significant intestinal hyperpermeability, and inosine exerted protective effect

62 vessels serves as a barrier against vascular hyperpermeability, and its maintenance is critical to or

63 in promoting lymphatic enlargement, vascular hyperpermeability, and leukocyte recruitment, thereby le

64 ernalization is required for agonist-induced hyperpermeability, and suggests that a mechanism by whic

65 ay was used to examine VEGF-induced vascular hyperpermeability, and the mouse corneal model of angiog

66 mitogen that promotes angiogenesis, vascular hyperpermeability, and vasodilation by autocrine mechani

67 Increased neovascularization and vascular hyperpermeability are integral processes in tumors, and

68 ular mechanisms by which VEGF acts to induce hyperpermeability are poorly understood and in vivo mode

69 Serous RD was not associated with hyperpermeability areas on ICGA.

70 de, cavtratin, was able to correct the tumor hyperpermeability as well as attenuate the increased tum

71 ulmonary alveolar epithelial and endothelial hyperpermeability as well as edema formation, all of whi

72 o attenuated Tat-induced endothelial and BBB hyperpermeability as well as transendothelial migration

73 dent biphasic blood flow stasis and vascular hyperpermeability, as determined by intravital microscop

74 n sulfate as a potential target for treating hyperpermeability associated with ischemic disease.

75 e were used to monitor dermal acute vascular hyperpermeability (AVH) and passive systemic anaphylaxis

76 BVP and the acute vascular hyperpermeability (AVH) induced by these vascular permea

77 re, as shown in Robo4(-/-) mice that develop hyperpermeability, but how Robo4 signals remained unclea

78 c injuries also promotes BBB dysfunction and hyperpermeability, but the underlying mechanisms are not

79 ith AICAR attenuated LPS-induced endothelial hyperpermeability by activating the Rac/Cdc42/PAK pathwa

80 drophobic statin, reversed VEGF-induced GEnC hyperpermeability by preventing MLC diphosphorylation, a

81 s essential to sustain organ health, chronic hyperpermeability causes damaging tissue edema.

82 VPF/VEGF induces vascular hyperpermeability, cell division, and other activities b

83 Chronic vascular hyperpermeability (CVH) was induced long before the onse

84 rotected EC monolayers from thrombin-induced hyperpermeability, disruption of intercellular junctions

85 orated the development of intestinal mucosal hyperpermeability during the reperfusion.

86 Increased expression of PDE2 can mediate hyperpermeability effects of paracrine endothelial NP/GC

87 Trpc1(-/-) mice resisted the hyperpermeability effects of the edemagenic agonists use

88 actor in the intrastrial fluid-blood barrier hyperpermeability exhibited in the mice is down-regulati

89 ts as a vasodilator, angiogenic peptide, and hyperpermeability factor.

90 ) breakdown and the associated microvascular hyperpermeability followed by brain edema are hallmark f

91 Sprague Dawley (SD) rats only showed retinal hyperpermeability from 3 to 10 days after the onset of d

92 hy (OIR), BN rats developed retinal vascular hyperpermeability from postnatal day 12 (P12) to P22 wit

93 requirement for heparan sulfate in vascular hyperpermeability has not been explored.

94 te prevented IgE-mediated cutaneous vascular hyperpermeability, hypothermia, elevation in plasma hist

95 bitor, L-NMMA, blocked VEGF-induced vascular hyperpermeability in all ocular and nonocular tissues, p

96 aled dilated choroidal vessels and choroidal hyperpermeability in areas corresponding to altered AF o

97 ored AJ integrity and diminished endothelial hyperpermeability in Cav-1(-/-) mice.

98 yline as a therapeutic inhibitor of vascular hyperpermeability in human clinical conditions is promis

99 d tumor necrosis factor (TNF)-alpha-mediated hyperpermeability in human umbilical vein endothelial ce

100 yielded additive reductions in CNV area and hyperpermeability in mice.

101 nctions with intercellular gap formation and hyperpermeability in microvascular endothelial cells.

102 JI-34 blunts PLY-mediated endothelial hyperpermeability in monolayers of HL-MVEC, in a cAMP-de

103 nduce formation of discrete foci of vascular hyperpermeability in premetastatic lungs.

104 in the signal transduction of microvascular hyperpermeability in response to growth factors and infl

105 nd prevented retinal cell death and vascular hyperpermeability in the diabetic retina.

106 st splanchnic reperfusion-induced intestinal hyperpermeability in the mouse.

107 orway (BN) rats developed sustained vascular hyperpermeability in the retina during the entire experi

108 e (AICAR) attenuated LPS-induced endothelial hyperpermeability in vitro.

109 paran sulfate-protein interactions inhibited hyperpermeability in vivo, suggesting heparan sulfate as

110 Sepsis induced intestinal hyperpermeability in wild-type mice compared with sham m

111 side counteracted lipopolysaccharide-induced hyperpermeability in wild-type mice in vivo as well as i

112 that a large component of pulmonary vascular hyperpermeability induced by activation of PMNs adherent

113 paran sulfate biosynthesis in vivo decreases hyperpermeability induced by both VEGF(165) and VEGF(121

114 vitro and in vivo and attenuates endothelial hyperpermeability induced by inflammatory and edemagenic

115 taining caveolae to plasma membrane inhibits hyperpermeability induced by platelet-activating factor

116 trate a previously unrecognized mechanism of hyperpermeability induced by rises in cytosolic cAMP.

117 lin-1 in VVO structure in the acute vascular hyperpermeability induced by VEGF-A and in pathological

118 bitors block proliferation and microvascular hyperpermeability induced by VEGF.

119 Transient vascular hyperpermeability, induced by histamine coinjection, exa

120 n strongly suppressed thrombin-induced HUVEC hyperpermeability, inhibiting ERK1/2 activation had no e

121 ling pathway that mediates VEGF-induced GEnC hyperpermeability involves RhoA activation leading to ac

122 A feature of thrombin-enhanced endothelial hyperpermeability is contraction of endothelial cells (E

123 ought to determine whether IFN-gamma-induced hyperpermeability is increased under acidic conditions.

124 Increased levels of knee swelling, hyperpermeability, leukocyte accumulation, and TNFalpha

125 s correlated with reduction of microvascular hyperpermeability, neutrophil infiltration, and endothel

126 ines, alveolar neutrophil accumulation, lung hyperpermeability, NO production, and lipid peroxidation

127 Vascular hyperpermeability occurred without apparent alteration i

128 y is controlled by CCR7 and that the chronic hyperpermeability of collecting vessels observed in Ccr7

129 e not involved in bradykinin- or PAF-induced hyperpermeability of intact microvessels.

130 tion of astrogliosis, neuroinflammation, and hyperpermeability of the blood-brain barrier.

131 igated whether mu-calpain is involved in the hyperpermeability of the diabetic vasculature.

132 The hyperpermeability of tumor vessels to macromolecules, co

133 modulates TNF-alpha-driven angiogenesis and hyperpermeability over time.

134 Pulmonary vascular hyperpermeability peaked 12 hrs postinjury and was relat

135 tor) successfully reversed the microvascular hyperpermeability phenotype of Cav-1 knock-out mice.

136 arget for limiting oxidant-mediated vascular hyperpermeability, protein-rich edema formation, and acu

137 immunoglobulins, the mechanisms of vascular hyperpermeability remain obscure.

138 d, thereby, contributes to the lung vascular hyperpermeability response during sepsis.

139 and vitronectin, respectively, prevented the hyperpermeability response to GRGDdSP and GPenGRGDSPCA.

140 Furthermore, the vascular hyperpermeability response to H(2)O(2) was completely re

141 ar endothelial monolayers, which displayed a hyperpermeability response to neutrophils and MLCK in a

142 l elements of the signalling pathway for the hyperpermeability response to PAF; (3) iNOS does not aff

143 a common role in mediating the microvascular hyperpermeability response to vascular endothelial growt

144 cific inhibiting peptide did not prevent the hyperpermeability response to VEGF or histamine.

145 n endothelial monolayers displayed a similar hyperpermeability response to VEGF which was greatly att

146 The hyperpermeability response was significantly attenuated

147 e course closely correlated with that of the hyperpermeability response.

148 rmation was observed in coincidence with the hyperpermeability response.

149 ut augmented RhoA activation and endothelial hyperpermeability response.

150 line permeability; (b) eNOS is essential for hyperpermeability responses in inflammation; and (c) mol

151 stration of AP-Cav blocked the microvascular hyperpermeability responses to 10(-7) m PAF.

152 s not affect either baseline permeability or hyperpermeability responses to PAF; and (4) caveolin-1 i

153 y prevented the VEGF-induced Ca2+ influx and hyperpermeability similar to the inhibitory effects seen

154 ence supports a role for an ischemia-induced hyperpermeability state regulated, in part, by VEGF.

155 xhibited higher ability to cause endothelial hyperpermeability than exosomes from the non metastatic

156 eas of previous or ongoing SRF and choroidal hyperpermeability that can assist in the diagnosis of CS

157 are characterized by abnormal morphology and hyperpermeability that together cause inefficient delive

158 that mediate endothelial barrier leakiness (hyperpermeability) that are important in the pathogenesi

159 on of Epac also counteracts thrombin-induced hyperpermeability through down-regulation of Rho GTPase

160 Because VEGF may signal endothelial hyperpermeability through the phospholipase C (PLC)-IP3

161 s on the induction of iNOS expression and/or hyperpermeability to hydrophilic solutes in cultured ent

162 r neovascularization and a state of vascular hyperpermeability to macromolecules.

163 Hyperpermeability triggered by inflammation or ischemia

164 rst time that CCL2 induces brain endothelial hyperpermeability via Rho/PKCalpha signal pathway intera

165 explored the hypothesis that PAF stimulates hyperpermeability via S-nitrosation (SNO) of adherens ju

166 oxidative stress-induced pulmonary vascular hyperpermeability via transcellular and paracellular pat

167 LPS-induced intestinal hyperpermeability was ameliorated by both aminoguanidine

168 The hyperpermeability was corrected with bisindolylmaleimide

169 The strain difference in vascular hyperpermeability was correlated with the different over

170 At 18 hours, acute hyperpermeability was measured with 125I-albumin, and cy

171 Such hyperpermeability was not rescued by inhibiting eNOS act

172 In OIR-SD rats, however, hyperpermeability was observed from P14 to P18, with a p

173 ipopolysaccharide-induced pulmonary vascular hyperpermeability was significantly reduced in CD44 knoc

174 Nonetheless, VEGF-A-induced hyperpermeability was strikingly reduced in cav-1(-/-) m

175 al models of acute lung injury with vascular hyperpermeability, we observed that HTJ-1 knockdown bloc

176 of acute lung injury with pulmonary vascular hyperpermeability, we observed that selective lung silen

177 Significantly less knee swelling and hyperpermeability were found in TRPV1-/- mice, but leuko

178 ction and of SNO blocked PAF-induced SNO and hyperpermeability, whereas inhibition of the cGMP pathwa

179 angiogenesis and associated chronic vascular hyperpermeability, whether induced by VEGF-A(164) or by

180 FU does not induce apoptosis rather vascular hyperpermeability, which can be alleviated by Resveratro

181 ndrome with diarrhea (IBS-D) have intestinal hyperpermeability, which contributes to their diarrhea a

182 Intestinal PARP activation resulted in gut hyperpermeability, which developed in PARP(+/+) but not

183 uced F-actin remodeling and Rho-dependent EC hyperpermeability, while expression of a phosphorylation

184 ICGA showed the characteristic choroidal hyperpermeability, while there was no evidence of choroi