コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ns are crucial for correct regulation of the endothelial barrier.
2 determined by their permeability across the endothelial barrier.
3 ility and contractility at the inner retinal endothelial barrier.
4 s comprising a sharp S1P gradient across the endothelial barrier.
5 abling inflammatory mediator flux across the endothelial barrier.
6 t lead to profound dysregulation of the lung endothelial barrier.
7 ers, resulting thereby in formation of leaky endothelial barrier.
8 s) are required for formation of restrictive endothelial barrier.
9 2+) stores, preventing the disruption of the endothelial barrier.
10 ing Ca(2+) entry-dependent disruption of the endothelial barrier.
11 ating recovery of the VE-cadherin-controlled endothelial barrier.
12 tating their transmigration of the lymphatic endothelial barrier.
13 ter and molecular tracers across the retinal endothelial barrier.
14 of adherens junctions, and disruption of the endothelial barrier.
15 eby establish the characteristic restrictive endothelial barrier.
16 passive movement of LDL across a compromised endothelial barrier.
17 aling and contribute to the integrity of the endothelial barrier.
18 emokines influencing the permeability of the endothelial barrier.
19 ncreased contractility and disruption of the endothelial barrier.
20 tion of VE-cadherin and for breakdown of the endothelial barrier.
21 1 controls membrane spreading and stabilizes endothelial barriers.
22 ctor by promoting invasion of epithelial and endothelial barriers.
23 that correlates with increased leakiness of endothelial barriers.
24 dly inhibited monocyte transmigration across endothelial barriers.
25 ling pathways regulating regeneration of the endothelial barrier after inflammatory vascular injury.
26 KBP51 axis to inhibit I(SOC) and protect the endothelial barrier against calcium entry-induced disrup
27 ncreased proficiency to transmigrate through endothelial barrier (an obligatory step for vascular dis
28 ry requires the reestablishment of an intact endothelial barrier and a functional alveolar epithelial
30 everity by damaging the pulmonary epithelial-endothelial barrier and increasing pulmonary oedema.
31 C) has previously been shown to tighten the endothelial barrier and maintain barrier integrity durin
32 e important for insulin transport across the endothelial barrier and mediate insulin's actions in mus
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 s been shown to control the integrity of the endothelial barrier and to support neutrophil transendot
36 circulating tumor cells must destabilize the endothelial barrier and transmigrate across the vessel w
37 through lymph nodes (LNs) requires crossing endothelial barriers and chemoattractant-triggered cell
38 ived APCs in the migration of T cells across endothelial barriers and have important implications for
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 n in vitro model of the pulmonary epithelial-endothelial barrier as well as an in vivo murine model o
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
47 ant link between abnormalities in PVM/Ms and endothelial barrier breakdown from acoustic trauma to th
51 rophil extravasation requires opening of the endothelial barrier but does not necessarily cause plasm
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
57 idate the KLF2-mediated pathways involved in endothelial barrier disruption and cytokine storm in exp
60 ress syndrome (ARDS) is caused by widespread endothelial barrier disruption and uncontrolled cytokine
65 e, head trauma, or high altitude can lead to endothelial barrier disruption referred to as capillary
66 We previously showed that thrombin promotes endothelial barrier disruption through autophosphorylati
74 roperty is central to the maintenance of the endothelial barrier during inflammation, the molecular m
75 hemolysis and free heme in circulation cause endothelial barrier dysfunction and are associated with
78 PK) in lipopolysaccharide (LPS)-induced lung endothelial barrier dysfunction and lung injury in vivo.
80 n of Src greatly attenuated nmMLCK-dependent endothelial barrier dysfunction and monocyte migration.
81 ted RhoA activation involved in LPS-mediated endothelial barrier dysfunction and show the potential u
84 indicated that nmMLCK deficiency attenuated endothelial barrier dysfunction caused by thrombin, oxid
89 endothelial monolayers, imatinib attenuated endothelial barrier dysfunction induced by thrombin and
93 1P effectively could reverse alcohol-induced endothelial barrier dysfunction using both cultured endo
94 ve kinases revealed that imatinib attenuates endothelial barrier dysfunction via inhibition of Abl-re
95 age of MEK1/2 was necessary for LT to induce endothelial barrier dysfunction, and activated Tie-2 sig
96 ility to attenuate LPS-induced inflammation, endothelial barrier dysfunction, and acute lung injury (
97 ng activation of coagulation and complement, endothelial barrier dysfunction, and microangiopathy.
105 keletal changes associated with S1P-mediated endothelial barrier enhancement and suggest a novel role
106 MT-actin cross talk mechanism of HGF-induced endothelial barrier enhancement and suggest that IQGAP1
107 osine 1-phosphate (S1P) produces significant endothelial barrier enhancement by means of peripheral a
108 tter understanding of mechanisms stimulating endothelial barrier enhancement may provide novel therap
109 Prostaglandin E receptor-4 receptor mediates endothelial barrier-enhancing and anti-inflammatory effe
110 This domain mediates establishment of the endothelial barrier; expression of the transmembrane dom
111 DN, while carrier-specific miRs can improve endothelial barrier formation (EV-miR-21/126) or exert a
112 nhibition both result in delayed recovery of endothelial barrier function after thrombin stimulation.
113 ofibroblast differentiation and contraction, endothelial barrier function and angiogenesis, and mesen
115 tery endothelial cells compromised pulmonary endothelial barrier function and enhanced their survival
116 e-TNF fusion product capable of altering the endothelial barrier function and improving drug penetrat
117 contributes to atherosclerosis by regulating endothelial barrier function and monocyte migration via
118 usion and blocked plasma leakage by enhanced endothelial barrier function and pericyte association wi
119 Disruption of tight junctions (TJs) perturbs endothelial barrier function and promotes inflammation.
120 R stress and O-GlcNAcylation in altering the endothelial barrier function and reveal a potential ther
121 enetrating CRADD protein (CP-CRADD) restored endothelial barrier function and suppressed the inductio
122 re, we demonstrate that CREB maintains basal endothelial barrier function and suppresses endothelial
123 conclude that AMPK activity supports normal endothelial barrier function and that LPS exposure inhib
124 injury, which is characterized by a loss of endothelial barrier function and the development of pulm
125 ver, mechanisms governing the restoration of endothelial barrier function are poorly understood.
127 le-positive areas further exhibited impaired endothelial barrier function as illuminated by Evans blu
128 y, maintains AJs and mitigates disruption of endothelial barrier function by edemagenic agents, there
129 hat initiates pericyte loss and breakdown of endothelial barrier function by generating the diol 19,2
131 uncover a pivotal role of CREB in regulating endothelial barrier function by restricting RhoA signali
136 probe in vivo mechanisms involving impaired endothelial barrier function in experimental atherothrom
137 of 62 members of the F-box protein family on endothelial barrier function in human umbilical vein end
138 at depletion of endogenous CRADD compromises endothelial barrier function in response to inflammatory
139 that gravin functionally couples to control endothelial barrier function in response to protein kina
140 ective role for the endocytic protein p18 in endothelial barrier function in settings of ALI in vitro
141 We conclude that p18 regulates pulmonary endothelial barrier function in vitro and in vivo, by en
143 enoic acid from arachidonic acid, decreasing endothelial barrier function in vitro In mice in vivo ph
151 different effects of these three agonists on endothelial barrier function occur independently of Ca(2
152 ingosine-1-phosphate-mediated enhancement of endothelial barrier function occurs independently of STI
154 serve to reverse vascular damage and restore endothelial barrier function through regeneration of a f
155 We show that S1P promotes cell spreading and endothelial barrier function through S1PR1-Galphai-Rac1
156 ssues is governed by mechanisms that control endothelial barrier function to maintain homeostasis.
162 opography significantly influence epithelial/endothelial barrier function where increased fiber stiff
163 ibe a new assay to dynamically measure local endothelial barrier function with a lateral resolution o
164 findings and other advances in understanding endothelial barrier function with the goal of identifyin
165 odeling is associated with a local change in endothelial barrier function, a direct proof is missing
167 ight junctions with a role in maintenance of endothelial barrier function, although how this is accom
168 y maintaining arterial integrity, preserving endothelial barrier function, and a normal contractile S
169 Moreover, Bmpr2(+/-) PECs have impaired endothelial barrier function, and barrier function is re
170 nists: thrombin and histamine, which disrupt endothelial barrier function, and sphingosine-1-phosphat
171 cell coverage on the endothelium and reduced endothelial barrier function, and this effect was abroga
172 ocalcin-1 inhibits macrophages and preserves endothelial barrier function, and transgenic overexpress
173 a homotypic adhesion molecule that regulates endothelial barrier function, and transmembrane chemokin
174 stress plays a critical role in maintaining endothelial barrier function, but how this occurs remain
175 B2/EphB4 signalling is dispensable for blood endothelial barrier function, but required for stabiliza
177 east as effective as SB203580 in stabilizing endothelial barrier function, reducing inflammation, and
178 gical functions, including key modulators of endothelial barrier function, regulators of gene transcr
179 ve and redundant roles in various aspects of endothelial barrier function, RhoB specifically inhibits
180 ify the contribution of the Asn-25 glycan to endothelial barrier function, we generated an N25Q mutan
219 erefore, enhancing drug transport across the endothelial barrier has to rely on leaky vessels arising
222 known how this signaling pathway affects the endothelial barrier in coherent ECs forming a tight mono
223 xpression of VEGFC compromised the lymphatic endothelial barrier in mice and endothelial cells, reduc
227 nduced TEM increase was not due to decreased endothelial barrier, increased adhesion molecule express
228 e mechanism to ensure timely transition from endothelial barrier injury to repair, accelerating barri
229 Endothelial cells have key functions in endothelial barrier integrity and in responses to angiog
230 ex partnering leading to the loss of retinal endothelial barrier integrity and increased transendothe
231 we investigated the role of free heme in the endothelial barrier integrity and mechanisms of heme-med
234 the endothelial cell surface, and decreased endothelial barrier integrity in vitro, therefore increa
237 ata indicate that matrix stiffness regulates endothelial barrier integrity through FAK activity, prov
238 CNS autoimmunity, the consequences on brain endothelial barrier integrity upon interaction with such
239 findings demonstrate that HIF2alpha enhances endothelial barrier integrity, in part through VE-PTP ex
240 NA-mediated down-regulation of Lyn disrupted endothelial barrier integrity, whereas expression of a c
250 ics activating Lyn kinase may strengthen the endothelial barrier junction and hence have anti-inflamm
251 ing a cross-talk between fibroblasts and the endothelial barrier leading to barrier opening, cellular
252 ewly defined signaling pathways that mediate endothelial barrier leakiness (hyperpermeability) that a
255 targeting neutrophil diapedesis through the endothelial barrier may represent a new therapeutic aven
256 tight- and adherens-junction proteins in the endothelial barrier of the stria vascularis (intrastrial
258 in-1 with a claudin-1 peptide improves brain endothelial barrier permeability and consequently functi
259 with a specific C1C2 peptide improved brain endothelial barrier permeability and functional recovery
260 o failed to protect against thrombin-induced endothelial barrier permeability in cells deficient in b
261 ide (LPS)-induced inflammatory responses and endothelial barrier permeability in human primary pulmon
262 38 activation was critical for PAR1-promoted endothelial barrier permeability in vitro, and p38 signa
263 l (VE)-cadherin homophilic adhesion controls endothelial barrier permeability through assembly of adh
264 metabolite of arachidonic acid (AA), induced endothelial barrier permeability via Src and Pyk2-depend
271 ascorbate in the prevention of inflammatory endothelial barrier permeabilization and explain the und
272 g RNA attenuated the HGF-induced increase in endothelial barrier properties and abolished HGF-activat
273 pendent kinase I (cGKI), strengthen systemic endothelial barrier properties in acute inflammation.
275 -2, which is critical for Rac1 signaling and endothelial barrier protection but not for thrombin-indu
280 observations have important implications for endothelial barrier regulation in glomerular and other m
283 e infiltration and reduced activation of the endothelial barrier regulator MLCK, and reduced phosphor
286 r translocation (~15%) across the co-culture endothelial barrier resulting in regression of tumor in
287 tricts tumor cell extravasation by enhancing endothelial barrier stability through modulation of mole
288 tial hits, of which, four compounds enhanced endothelial barrier stability while concurrently suppres
289 VIIIa; (2) a cytoprotective on the basis of endothelial barrier stabilization and anti-inflammatory
291 afficking to facilitate dissemination across endothelial barriers such as the blood-brain barrier.
293 that it is neutrophil diapedesis through the endothelial barrier that is responsible for the bleeding
294 cytes contribute to cellular interactions at endothelial barriers that impart protective CNS inflamma
295 bioenergetics and failure of epithelial and endothelial barriers that produce organ dysfunction and
296 adherin homophilic interaction in modulating endothelial barrier through the tuning of MT dynamics.
298 An example is drug carriers targeted to endothelial barriers, which can be transported to intra-
299 er demonstrate a protective role for TNAP at endothelial barriers within this axis, transgenic mice w
300 vascular endothelial cAMP and stabilize the endothelial barrier would attenuate the action of endoge