ライフサイエンスコーパス: endothelial barrier

1 t lead to profound dysregulation of the lung endothelial barrier.

2 ers, resulting thereby in formation of leaky endothelial barrier.

3 determined by their permeability across the endothelial barrier.

4 s) are required for formation of restrictive endothelial barrier.

5 2+) stores, preventing the disruption of the endothelial barrier.

6 ing Ca(2+) entry-dependent disruption of the endothelial barrier.

7 ating recovery of the VE-cadherin-controlled endothelial barrier.

8 tating their transmigration of the lymphatic endothelial barrier.

9 ter and molecular tracers across the retinal endothelial barrier.

10 of adherens junctions, and disruption of the endothelial barrier.

11 herens junctions (AJs) to form a restrictive endothelial barrier.

12 portant for maintaining the integrity of the endothelial barrier.

13 ed to activate Rac1 and Cdc42 or protect the endothelial barrier.

14 r activates its receptor S1P1 to restore the endothelial barrier.

15 ular event responsible for the disruption of endothelial barrier.

16 ence in contributing to the leakiness of the endothelial barrier.

17 ility and contractility at the inner retinal endothelial barrier.

18 s comprising a sharp S1P gradient across the endothelial barrier.

19 abling inflammatory mediator flux across the endothelial barrier.

20 tion of VE-cadherin and for breakdown of the endothelial barrier.

21 ctor by promoting invasion of epithelial and endothelial barriers.

22 1 controls membrane spreading and stabilizes endothelial barriers.

23 s that have been implicated in S1P-dependent endothelial barrier activity.

24 ling pathways regulating regeneration of the endothelial barrier after inflammatory vascular injury.

25 ncreased proficiency to transmigrate through endothelial barrier (an obligatory step for vascular dis

26 ry requires the reestablishment of an intact endothelial barrier and a functional alveolar epithelial

27 echanisms by which this pathogen crosses the endothelial barrier and establishes new sites of infecti

28 in mice lungs that led to the disruption of endothelial barrier and lung edema formation; however, t

29 tion may be beneficial in reestablishing the endothelial barrier and lung fluid balance in lung infla

30 C) has previously been shown to tighten the endothelial barrier and maintain barrier integrity durin

31 e important for insulin transport across the endothelial barrier and mediate insulin's actions in mus

32 trophils (PMNs) receive signals to cross the endothelial barrier and migrate through the extracellula

33 ights into the biomechanical function of the endothelial barrier and suggests similar opportunities f

34 escribe a new mechanism regulating the tumor endothelial barrier and T cell infiltration into tumors.

35 through lymph nodes (LNs) requires crossing endothelial barriers and chemoattractant-triggered cell

36 ived APCs in the migration of T cells across endothelial barriers and have important implications for

37 re resulted in increased permeability of the endothelial barrier, and this effect was abrogated in mi

38 H(2)S transport through epithelial barriers, endothelial barriers, and membrane rafts also occurs by

39 /165 and VEGF165b in both brain and nonbrain endothelial barrier, angiogenesis, and neutrophil migrat

40 on of inflammatory cells across the vascular endothelial barrier are crucial factors in the pathogene

41 t demonstrated increased permeability of the endothelial barrier as evidenced by Evans blue and sodiu

42 acquire lumican during or after crossing the endothelial barrier as they exit circulation.

43 on of human neutrophils to inflamed vascular endothelial barriers as well as their subsequent transmi

44 (Th17) lymphocyte transmigration across the endothelial barrier at the expense of T regulatory cells

45 increase endothelial cAMP and stabilize the endothelial barrier attenuates acute inflammatory increa

46 Defects in the endothelial barrier become an initiating factor in sever

47 The integrity of the endothelial barrier between circulating blood and tissue

48 ant link between abnormalities in PVM/Ms and endothelial barrier breakdown from acoustic trauma to th

49 and adherens junction disassembly leading to endothelial barrier breakdown.

50 fection leading to systemic inflammation and endothelial barrier breakdown.

51 s that suppress apoptosis, inflammation, and endothelial barrier breakdown.

52 to extravasate across a permeable capillary endothelial barrier, but not with gadofosveset, a blood-

53 of focal adherens junctions, disrupting the endothelial barrier by acting on H1R Galphaq-coupled rec

54 acity to promote tumor cell invasion through endothelial barriers by both direct and indirect mechani

55 st phase but ameliorated the second phase of endothelial barrier disruption and apoptosis.

56 idate the KLF2-mediated pathways involved in endothelial barrier disruption and cytokine storm in exp

57 in mediating VE-cadherin internalization and endothelial barrier disruption and inflammation.

58 Lung vascular endothelial barrier disruption and the accompanying infl

59 ress syndrome (ARDS) is caused by widespread endothelial barrier disruption and uncontrolled cytokine

60 o-inflammatory chemokine CCL2 mediates brain endothelial barrier disruption during CNS inflammation.

61 nitro-L-arginine methyl ester attenuated the endothelial barrier disruption in both phases.

62 Endothelial barrier disruption is a hallmark of multiple

63 Importantly, CS-induced endothelial barrier disruption was attenuated by VEGFR2

64 the recovery process after thrombin-induced endothelial barrier disruption.

65 adherin/beta-catenin complexes and resultant endothelial barrier disruption.

66 rough the membrane I(SOC) channel leading to endothelial barrier disruption.

67 s that regulates endosomal p38 signaling and endothelial barrier disruption.

68 Due to disruption of the endothelial barrier during cold-ischemic storage and rep

69 roperty is central to the maintenance of the endothelial barrier during inflammation, the molecular m

70 emorrhagic fever (DHF) are largely caused by endothelial barrier dysfunction and a unique vascular le

71 Thus, imatinib prevents endothelial barrier dysfunction and edema formation via

72 Here, we explored the effect of imatinib on endothelial barrier dysfunction and edema formation.

73 PK) in lipopolysaccharide (LPS)-induced lung endothelial barrier dysfunction and lung injury in vivo.

74 osure inhibits AMPK, thereby contributing to endothelial barrier dysfunction and lung injury.

75 n of Src greatly attenuated nmMLCK-dependent endothelial barrier dysfunction and monocyte migration.

76 ted RhoA activation involved in LPS-mediated endothelial barrier dysfunction and show the potential u

77 Tissue edema and endothelial barrier dysfunction as observed in sepsis an

78 Imatinib limited Arg-mediated endothelial barrier dysfunction by enhancing Rac1 activi

79 indicated that nmMLCK deficiency attenuated endothelial barrier dysfunction caused by thrombin, oxid

80 Thus, endothelial barrier dysfunction due to 3MC occurs throug

81 Cs and that this may contribute to pulmonary endothelial barrier dysfunction in HPAH patients.

82 Protein nitration is involved in the endothelial barrier dysfunction in LPS-exposed mice.

83 Inhibiting RhoA signaling restored endothelial barrier dysfunction in the dn-CREB-expressin

84 endothelial monolayers, imatinib attenuated endothelial barrier dysfunction induced by thrombin and

85 -inflammatory responses and protects against endothelial barrier dysfunction induced by thrombin.

86 Endothelial barrier dysfunction leading to increased per

87 Endothelial barrier dysfunction underlies chronic inflam

88 Vascular endothelial barrier dysfunction underlies diseases such

89 1P effectively could reverse alcohol-induced endothelial barrier dysfunction using both cultured endo

90 ve kinases revealed that imatinib attenuates endothelial barrier dysfunction via inhibition of Abl-re

91 age of MEK1/2 was necessary for LT to induce endothelial barrier dysfunction, and activated Tie-2 sig

92 ility to attenuate LPS-induced inflammation, endothelial barrier dysfunction, and acute lung injury (

93 ng activation of coagulation and complement, endothelial barrier dysfunction, and microangiopathy.

94 of alternative signaling pathways mediating endothelial barrier dysfunction, dependent upon thrombin

95 icant potentiation of LPS-induced human lung endothelial barrier dysfunction, which was attenuated by

96 (Arg/Abl2), a previously unknown mediator of endothelial barrier dysfunction.

97 infiltration into the liver and kidney, and endothelial barrier dysfunction.

98 lular distribution were conducted to examine endothelial barrier dysfunction.

99 tal targets have been implicated in vascular endothelial barrier dysfunction; however, the immediate

100 keletal changes associated with S1P-mediated endothelial barrier enhancement and suggest a novel role

101 MT-actin cross talk mechanism of HGF-induced endothelial barrier enhancement and suggest that IQGAP1

102 osine 1-phosphate (S1P) produces significant endothelial barrier enhancement by means of peripheral a

103 tter understanding of mechanisms stimulating endothelial barrier enhancement may provide novel therap

104 Prostaglandin E receptor-4 receptor mediates endothelial barrier-enhancing and anti-inflammatory effe

105 Furthermore, the anionic sites at glomerular endothelial barrier estimated by cationic ferritin bindi

106 This domain mediates establishment of the endothelial barrier; expression of the transmembrane dom

107 nhibition both result in delayed recovery of endothelial barrier function after thrombin stimulation.

108 We identified that improvement of endothelial barrier function along with impaired neutrop

109 ofibroblast differentiation and contraction, endothelial barrier function and angiogenesis, and mesen

110 0), which is required for IGPR-1 to regulate endothelial barrier function and angiogenesis.

111 receptor 1 (PAR1), an important regulator of endothelial barrier function and blood coagulation, has

112 tery endothelial cells compromised pulmonary endothelial barrier function and enhanced their survival

113 e-TNF fusion product capable of altering the endothelial barrier function and improving drug penetrat

114 contributes to atherosclerosis by regulating endothelial barrier function and monocyte migration via

115 usion and blocked plasma leakage by enhanced endothelial barrier function and pericyte association wi

116 DS AND We observed that BMPCs enhanced basal endothelial barrier function and prevented the increase

117 Disruption of tight junctions (TJs) perturbs endothelial barrier function and promotes inflammation.

118 enetrating CRADD protein (CP-CRADD) restored endothelial barrier function and suppressed the inductio

119 re, we demonstrate that CREB maintains basal endothelial barrier function and suppresses endothelial

120 conclude that AMPK activity supports normal endothelial barrier function and that LPS exposure inhib

121 injury, which is characterized by a loss of endothelial barrier function and the development of pulm

122 ver, mechanisms governing the restoration of endothelial barrier function are poorly understood.

123 A group of proteins that that control the endothelial barrier function are the RhoGTPases.

124 le-positive areas further exhibited impaired endothelial barrier function as illuminated by Evans blu

125 ory and antiapoptotic effects and stabilizes endothelial barrier function by APC-initiated cell signa

126 y, maintains AJs and mitigates disruption of endothelial barrier function by edemagenic agents, there

127 hat initiates pericyte loss and breakdown of endothelial barrier function by generating the diol 19,2

128 We propose that p110alpha regulates endothelial barrier function by inducing the formation o

129 Regulation of brain endothelial barrier function by microRNAs in health and

130 A metabolism critically determines pulmonary endothelial barrier function by modulating Rac1-mediated

131 hereas activation of Rac1 and Cdc42 enhances endothelial barrier function by promoting the formation

132 uncover a pivotal role of CREB in regulating endothelial barrier function by restricting RhoA signali

133 Furthermore, miR-155 modulated brain endothelial barrier function by targeting not only cell-

134 However, disruption of endothelial barrier function by thrombin and histamine r

135 profoundly reduced their capacity to promote endothelial barrier function ex vivo.

136 Impaired endothelial barrier function in apolipoprotein M-deficie

137 probe in vivo mechanisms involving impaired endothelial barrier function in experimental atherothrom

138 , could mediate RhoA-dependent disruption of endothelial barrier function in mouse lungs during ALI.

139 laminohydrolases (DDAH) in the regulation of endothelial barrier function in pulmonary macrovascular

140 at depletion of endogenous CRADD compromises endothelial barrier function in response to inflammatory

141 that gravin functionally couples to control endothelial barrier function in response to protein kina

142 ective role for the endocytic protein p18 in endothelial barrier function in settings of ALI in vitro

143 motility, a process that may also relate to endothelial barrier function in the context of a vascula

144 re markedly efficient and did not compromise endothelial barrier function in vitro (determined by imm

145 We conclude that p18 regulates pulmonary endothelial barrier function in vitro and in vivo, by en

146 We evaluated the effect of imatinib on endothelial barrier function in vitro and in vivo.

147 enoic acid from arachidonic acid, decreasing endothelial barrier function in vitro In mice in vivo ph

148 Regulation of endothelial barrier function is critical for vascular ho

149 Understanding endothelial barrier function is critical for vascular ho

150 Impairment of endothelial barrier function is implicated in many vascu

151 Endothelial barrier function is regulated by adherens ju

152 Endothelial barrier function is tightly regulated by pla

153 However, the role of CREB in regulating endothelial barrier function is unknown.

154 different effects of these three agonists on endothelial barrier function occur independently of Ca(2

155 ingosine-1-phosphate-mediated enhancement of endothelial barrier function occurs independently of STI

156 Impaired endothelial barrier function results in a persistent inc

157 We show that S1P promotes cell spreading and endothelial barrier function through S1PR1-Galphai-Rac1

158 Improved endothelial barrier function toward the entry of plasma

159 Endothelial barrier function was determined based on ele

160 Endothelial barrier function was promoted by CXCL12/CXCR

161 opography significantly influence epithelial/endothelial barrier function where increased fiber stiff

162 Endothelial barrier function, a functional correlate of

163 y maintaining arterial integrity, preserving endothelial barrier function, and a normal contractile S

164 Moreover, Bmpr2(+/-) PECs have impaired endothelial barrier function, and barrier function is re

165 endothelial cells, severe impairment of the endothelial barrier function, and finally, disintegratio

166 nists: thrombin and histamine, which disrupt endothelial barrier function, and sphingosine-1-phosphat

167 cell coverage on the endothelium and reduced endothelial barrier function, and this effect was abroga

168 ocalcin-1 inhibits macrophages and preserves endothelial barrier function, and transgenic overexpress

169 a homotypic adhesion molecule that regulates endothelial barrier function, and transmembrane chemokin

170 stress plays a critical role in maintaining endothelial barrier function, but how this occurs remain

171 phosphoinositide 3-kinases (PI3Ks) increase endothelial barrier function, but the roles of different

172 Sphingosine-1-phosphate (S1P) can regulate endothelial barrier function, but the sources of the S1P

173 nic agents in restoring pre-injury levels of endothelial barrier function, following the establishmen

174 for p18 in VE-cadherin trafficking and thus endothelial barrier function, in settings of ALI.

175 east as effective as SB203580 in stabilizing endothelial barrier function, reducing inflammation, and

176 ve and redundant roles in various aspects of endothelial barrier function, RhoB specifically inhibits

177 ify the contribution of the Asn-25 glycan to endothelial barrier function, we generated an N25Q mutan

178 ulating LIMK1 may lead to the enhancement of endothelial barrier function, which could protect mice f

179 E disease severity as the result of enhanced endothelial barrier function.

180 y ecto-5'-nucleotidase (CD73) helps maintain endothelial barrier function.

181 ng molecule active in immune homeostasis and endothelial barrier function.

182 coagulation, inflammation, and disruption of endothelial barrier function.

183 Rap1-effector involved in cell spreading and endothelial barrier function.

184 ood facilitates tumor metastasis by relaxing endothelial barrier function.

185 actin dynamics, through which Rap1 modulates endothelial barrier function.

186 ion of endothelial junctions, which controls endothelial barrier function.

187 ically coordinated during cell spreading and endothelial barrier function.

188 d internal cellular tension led to decreased endothelial barrier function.

189 y strategy to prevent disruption of vascular endothelial barrier function.

190 al-cadherin cleavage and concomitant loss of endothelial barrier function.

191 s selective calcium permeation important for endothelial barrier function.

192 -time imaging, and precise quantification of endothelial barrier function.

193 tribute to vascular inflammation by altering endothelial barrier function.

194 utility of FRAP as a quantitative measure of endothelial barrier function.

195 lood vasculature, consistent with defects in endothelial barrier function.

196 ng VE-cadherin expression and the control of endothelial barrier function.

197 LF4 in regulating VE-cadherin expression and endothelial barrier function.

198 d in the acquisition of VE-cadherin-mediated endothelial barrier function.

199 nt to that in human CCM, results in impaired endothelial barrier function.

200 ng of the molecular mechanisms governing the endothelial barrier function.

201 r SPHK1-deficient endothelial cells restored endothelial barrier function.

202 n molecule VE-cadherin, thereby rescuing the endothelial barrier function.

203 signaling is required for receptor-regulated endothelial barrier function.

204 signaling and changes in human microvascular endothelial barrier function.

205 CR agonists that either disrupt or stabilize endothelial barrier function.

206 VE)-cadherin, resulting in the disruption of endothelial barrier function.

207 lar endothelial cells (ECs) and may regulate endothelial barrier function.

208 oted AJ integrity, and prevented the loss of endothelial barrier function.

209 tosis and thereby augmented AJ integrity and endothelial barrier function.

210 othelial NP/GC-A/cGMP/PDE2 signaling impairs endothelial barrier functions.

211 erefore, enhancing drug transport across the endothelial barrier has to rely on leaky vessels arising

212 ant role for FGF signaling in maintenance of endothelial barrier homeostasis through the regulation o

213 mediators in endothelial cells in regulating endothelial barrier homeostasis.

214 ot mediated by CaMKII and is not involved in endothelial barrier hyperpermeability.

215 We found that endothelial barrier impairment was associated with a hig

216 on of tumor necrosis factor alpha results in endothelial barrier impairment.

217 xpression of VEGFC compromised the lymphatic endothelial barrier in mice and endothelial cells, reduc

218 in-5) in increased permeability of the brain endothelial barrier in vitro.

219 tivation of TRPV4 channels regulates retinal endothelial barriers in vitro and in vivo.

220 CD4(+) T cells into the CNS and across brain endothelial barriers in vitro.

221 CXCR7 expression on endothelial barriers increased during EAE at sites of in

222 KLF4 knockdown disrupted the endothelial barrier, indicating that KLF4 is required fo

223 e mechanism to ensure timely transition from endothelial barrier injury to repair, accelerating barri

224 Here we show that HDL increases endothelial barrier integrity as measured by electric ce

225 ific regulation of Rac1 trafficking controls endothelial barrier integrity during inflammation.

226 Here we report that maintenance of endothelial barrier integrity during leukocyte diapedesi

227 the endothelial cell surface, and decreased endothelial barrier integrity in vitro, therefore increa

228 or agonists alter lymphocyte trafficking and endothelial barrier integrity in vivo.

229 ine protease, which causes the local loss of endothelial barrier integrity thereby enabling the rapid

230 CNS autoimmunity, the consequences on brain endothelial barrier integrity upon interaction with such

231 findings demonstrate that HIF2alpha enhances endothelial barrier integrity, in part through VE-PTP ex

232 NA-mediated down-regulation of Lyn disrupted endothelial barrier integrity, whereas expression of a c

233 hanisms and its role in maintaining vascular endothelial barrier integrity.

234 the opposing functions of these proteases on endothelial barrier integrity.

235 orectal tumors in mice and reduces lymphatic endothelial barrier integrity.

236 whereas other blood cells readily cross the endothelial barrier into the circulation.

237 CXCL12, is essential for leukocyte entry via endothelial barriers into the central nervous system (CN

238 The permeability of the endothelial barrier is an exquisitely regulated process

239 During metastasis, breakdown of the endothelial barrier is critical for tumor cell extravasa

240 how histamine induces the disruption of the endothelial barrier is not well defined.

241 Permeability of the endothelial barrier is primarily regulated by a protein

242 ics activating Lyn kinase may strengthen the endothelial barrier junction and hence have anti-inflamm

243 increased phosphorylation of VE-cadherin and endothelial barrier leakage.

244 ewly defined signaling pathways that mediate endothelial barrier leakiness (hyperpermeability) that a

245 telet-activating factor (PAF) induces severe endothelial barrier leakiness, but the signaling mechani

246 ntegrates FAK with AJ, preventing persistent endothelial barrier leakiness.

247 The endothelial barrier maintains vascular and tissue homeos

248 targeting neutrophil diapedesis through the endothelial barrier may represent a new therapeutic aven

249 , and found that these cells both invaded an endothelial barrier more efficiently and exhibited enhan

250 opulation of cells, TEM4-18, that crossed an endothelial barrier more efficiently, but surprisingly,

251 tight- and adherens-junction proteins in the endothelial barrier of the stria vascularis (intrastrial

252 165 nor VEGF165b significantly altered brain endothelial barrier or angiogenesis in vitro.

253 uced extravascular lung water, improved lung endothelial barrier permeability and restored alveolar f

254 o failed to protect against thrombin-induced endothelial barrier permeability in cells deficient in b

255 38 activation was critical for PAR1-promoted endothelial barrier permeability in vitro, and p38 signa

256 l (VE)-cadherin homophilic adhesion controls endothelial barrier permeability through assembly of adh

257 protease, induces inflammatory responses and endothelial barrier permeability through the activation

258 metabolite of arachidonic acid (AA), induced endothelial barrier permeability via Src and Pyk2-depend

259 olecular and signaling mechanisms regulating endothelial barrier permeability with emphasis on the cr

260 , small GTPases that differentially regulate endothelial barrier permeability.

261 EPCR), a protein involved in coagulation and endothelial barrier permeability.

262 nist-induced phosphoinositide hydrolysis and endothelial barrier permeability.

263 r p38 activation used by PAR1 that regulates endothelial barrier permeability.

264 nterendothelial junction (IEJ), causes acute endothelial barrier permeability.

265 ascorbate in the prevention of inflammatory endothelial barrier permeabilization and explain the und

266 Together, the findings indicate that HDL has endothelial barrier promoting activities, which are attr

267 g RNA attenuated the HGF-induced increase in endothelial barrier properties and abolished HGF-activat

268 pendent kinase I (cGKI), strengthen systemic endothelial barrier properties in acute inflammation.

269 sphocholine) significantly enhances vascular endothelial barrier properties in vitro and in vivo and

270 n of tight junction (TJ) gene expression and endothelial barrier properties.

271 -2, which is critical for Rac1 signaling and endothelial barrier protection but not for thrombin-indu

272 Strikingly, APC signaling and endothelial barrier protection effects were abolished in

273 ed C3 botulinum toxin substrate 1 (Rac1) and endothelial barrier protection.

274 C selective signaling to Rac1 activation and endothelial barrier protection.

275 Thus, APC selective signaling and endothelial barrier protective effects are mediated thro

276 Endothelial barrier protective effects of activated prot

277 We also tested the hypothesis that an endothelial barrier-protective bioactive lipid, sphingos

278 t those beginning at amino acid 39, conveyed endothelial barrier-protective effects.

279 wn about mechanisms by which FoxM1 regulates endothelial barrier reannealing.

280 etion triggered Gbeta1 activation of FAK and endothelial barrier recovery, whereas Fyn knockdown inte

281 observations have important implications for endothelial barrier regulation in glomerular and other m

282 up-regulation of Rac signaling critical for endothelial barrier regulation.

283 improve our understanding on human pulmonary endothelial barrier regulation.

284 Platelet intoxication prevents endothelial barrier repair and facilitates formation of

285 thelial cell migration, suggesting a role in endothelial barrier repair.

286 Repair of a dysfunctional endothelial barrier requires controlled restoration of a

287 ion, depletion of zyxin resulted in delay of endothelial barrier restoration after thrombin treatment

288 blood flow through mucosal microvessels, an endothelial "barrier," sensory innervation, and generati

289 VIIIa; (2) a cytoprotective on the basis of endothelial barrier stabilization and anti-inflammatory

290 esenting a novel target for preventing leaky endothelial barrier syndrome.

291 rier system in invertebrates evolved into an endothelial barrier system.

292 that it is neutrophil diapedesis through the endothelial barrier that is responsible for the bleeding

293 cytes contribute to cellular interactions at endothelial barriers that impart protective CNS inflamma

294 bioenergetics and failure of epithelial and endothelial barriers that produce organ dysfunction and

295 adherin homophilic interaction in modulating endothelial barrier through the tuning of MT dynamics.

296 dothelial AJs in order to form a restrictive endothelial barrier through transcriptional control of b

297 r tone at vascular endothelial and lymphatic endothelial barriers, through which S1P agonism impacts

298 ium prepared from the stressed OPCs weakened endothelial barrier tightness in vitro.

299 Stabilizing the endothelial barrier to offset ANP-induced increases in v

300 vascular endothelial cAMP and stabilize the endothelial barrier would attenuate the action of endoge