ライフサイエンスコーパス: paracellular

1 icating that it is predominantly passive and paracellular.

2 iated intercellular barrier and facilitating paracellular absorption of BoNT/A.

3 mulation and biotransformation combined with paracellular and active transport.

4 Brain endothelial cells form a paracellular and transcellular barrier to many blood-bor

5 port spermatogenesis and effectively enhance paracellular and transcellular diffusion of drugs (e.g.,

6 ncreased mortality, yet the contributions of paracellular and transcellular mechanisms to this proces

7 es revealed that molecules permeate via both paracellular and transcellular pathways in the presence

8 ormal tissues and in solid tumors, including paracellular and transcellular pathways that enable pass

9 rease in the water filtration coefficient of paracellular and transcellular pathways, and a decrease

10 to the tubular lumen, as well as in coupling paracellular and transcellular sodium permeability.

11 idney have different abilities to facilitate paracellular and transcellular transport of water and so

12 utilizes a nanoscale pipet to differentiate paracellular and transcellular transport processes at hi

13 ght junction strands and constitute both the paracellular barrier and the pore.

14 There was a paracellular barrier defect in rat epidermal keratinocyt

15 face carbohydrates, and HA2-HA3, involved in paracellular barrier disruption by E-cadherin binding.

16 s provide new insight into the mechanisms of paracellular barrier formation by demonstrating that def

17 Claudins have a paracellular barrier function.

18 markedly disrupted, resulting in the loss of paracellular barrier function.

19 important BBB property is the formation of a paracellular barrier made by tight junctions (TJs) betwe

20 wise impairment of transcellular followed by paracellular barrier mechanisms accounts for the BBB def

21 ls have reduced vessel density but increased paracellular barrier permeability.

22 CPE-mediated damage was enhanced if paracellular barrier was impaired by Ca2+ depletion, pro

23 Their presence generates a paracellular barrier, analogous to animal tight junction

24 roteins that are essential components of the paracellular barrier.

25 ogenous mechanism controlling the intestinal paracellular barrier.

26 r mutant epithelia fail to form an effective paracellular barrier.

27 uantity and type of molecules that cross the paracellular barrier.

28 This limits the molecular understanding of paracellular barriers and strategies for drug delivery a

29 specific claudin subtypes related either to paracellular barriers that impede drug delivery or to tu

30 ve degradation of tight junction proteins or paracellular BBB leakage.

31 Thus, apoM-bound S1P maintains low paracellular BBB permeability in all cerebral microvesse

32 eceptor 1 agonist SEW2871 rapidly normalized paracellular BBB permeability in Apom(-/-) mice, and inh

33 c cell lines, supporting the hypothesis that paracellular bile leakage through deficient TJs is invol

34 permeability and liver injuries secondary to paracellular bile regurgitation.

35 gnaling pathway in the kidney that underlies paracellular Ca(++) reabsorption through the tight junct

36 udin14 (Cldn14), an inhibitory factor of the paracellular Ca(2+) transport in the TAL, was significan

37 naling directly and indirectly regulates the paracellular Ca(2+) transport pathway by modulating Cldn

38 reasing the lumen-positive driving force for paracellular Ca(2+) transport.

39 and NEDD4L expression, as well as decreased paracellular calcium and magnesium reabsorption.

40 physical interaction, claudin-14 blocks the paracellular cation channel made of claudin-16 and -19,

41 hat HDAC inhibitors transiently increase the paracellular cation conductance in the thick ascending l

42 lation of Claudin14, a negative regulator of paracellular cation permeability in the thick ascending

43 lation of Claudin16, a positive regulator of paracellular cation permeability.

44 nctions, both claudin-2 and claudin-10b form paracellular cation-selective pores by the interaction o

45 bryonic than the postnatal stages, acts as a paracellular channel for small cations, such as Na(+), s

46 tes renal Ca(++) handling through changes in paracellular channel permeability in the thick ascending

47 passage of small and larger solutes by both paracellular channel-based and some additional mechanism

48 is (FHHNC) was previously considered to be a paracellular channelopathy caused by mutations in the cl

49 Claudin-2 forms gated paracellular channels and allows sodium ions and other s

50 We conclude that claudin-2 forms gated paracellular channels and speculate that modulation of t

51 In addition, certain claudins function as paracellular channels for small ions and/or solutes by f

52 of at least two spatially distinct types of paracellular channels in TAL: a cldn10b-based channel fo

53 cells migrated into the lumen moving through paracellular channels within the epithelium.

54 he claudin-8 interaction with claudin-4, the paracellular chloride channel, and delocalization of cla

55 knockdown of KLHL3 profoundly increased the paracellular chloride permeability.

56 The paracellular claudin channel of the thick ascending limb

57 tant endothelial cells precociously form the paracellular component of the barrier.

58 t has been hypothesized that VECs facilitate paracellular diapedesis by opening their cell-cell junct

59 unctional gaps in the endothelial monolayer (paracellular diapedesis).

60 he sequence of mechanical events involved in paracellular diapedesis.

61 cells and are responsible for regulation of paracellular diffusion and maintenance of cellular polar

62 ateral cell surface domains that serves as a paracellular diffusion barrier, enabling epithelial cell

63 relation was observed between G, an index of paracellular diffusion of ions, and mannitol permeabilit

64 ity to intact 33-mer or p31-49 did not favor paracellular diffusion of the peptides.

65 These barriers inhibit paracellular diffusion, thereby protecting the CNS from

66 Although TJs are known to regulate paracellular diffusion, this barrier function has not be

67 s at low frequencies, indicative of a higher paracellular electrical impedance with respect to the st

68 tilization in the kidney may be supported by paracellular epithelial transport, a form of passive dif

69 rming that junctional disruption resulted in paracellular exchange between the blood stream and the b

70 Blood-brain barrier pericytes regulate paracellular flow between cells, transendothelial fluid

71 ined by tight junction proteins that control paracellular fluid flux.

72 ated knockout of TOCA-1 results in increased paracellular flux and delayed recovery in a calcium swit

73 ue to measure intestinal permeability, using paracellular flux and electrical measurements.

74 dy transepithelial electrical resistance and paracellular flux of fluorescein isothiocyanate-dextran

75 asure transepithelial electrical resistance, paracellular flux of fluorescein isothiocyanate-dextran

76 TNF increased paracellular flux of large molecules in occludin-suffici

77 eakage, which was characterized by increased paracellular flux of small molecules and was associated

78 nt collecting duct cells displayed increased paracellular flux of sodium, chloride, and urea.

79 ons are cell-cell contacts that regulate the paracellular flux of solutes and prevent pathogen entry

80 to disrupt tight junctions, and this permits paracellular flux of toxin.

81 ed to effector caspase activation, increased paracellular flux, and redistribution of zonula occluden

82 is of transepithelial electrical resistance, paracellular flux, mRNA expression, Western blotting, an

83 rt of phosphate in jejunum, without changing paracellular fluxes.

84 al membrane potential, and transcellular and paracellular fluxes.

85 Similar enhanced rates of paracellular glucose flux were also observed across exci

86 lial monolayers to PIMs results in increased paracellular glucose flux, as well as apical GLUT-mediat

87 ncreases towards that of basolateral liquid, paracellular HCO(3) (-) flux becomes absorptive, temperi

88 ular HCO(3) (-) permeability, and calculated paracellular HCO(3) (-) flux was absorptive.

89 ed paracellular HCO(3) (-) permeability, and paracellular HCO(3) (-) flux was negligible.

90 Under basal conditions, calculated paracellular HCO(3) (-) flux was secretory.

91 nder basal conditions at pH ~6.6, calculated paracellular HCO(3) (-) flux was weakly secretory.

92 However, there is limited information about paracellular HCO(3) (-) flux, and it remains uncertain w

93 rway surface liquid pH decreased or reversed paracellular HCO(3) (-) flux.

94 13 increased ASL pH to ~7.4 without altering paracellular HCO(3) (-) permeability, and calculated par

95 Falpha alkalinized ASL pH to ~7.0, increased paracellular HCO(3) (-) permeability, and paracellular H

96 To investigate paracellular HCO(3) (-) transport, we studied differenti

97 shift from paracellular sodium transport to paracellular hyperabsorption of calcium and magnesium.

98 Such paracellular ice penetration occurred in the majority of

99 s used to quantify the rate constants of the paracellular ice penetration process, the penetration-as

100 Paracellular ice penetration was generally not observed

101 Magnesium absorption is mainly paracellular in the proximal tubule and in the thick asc

102 lities of all pathways (apical, basolateral, paracellular) in human nasal epithelia cultures using ex

103 role in asthma pathogenesis by enabling the paracellular influx of allergens, toxins, and microbes t

104 monstrated that SPAK significantly increased paracellular intestinal permeability to FITC-dextran.

105 -junction transmembrane proteins that act as paracellular ion channels in epithelial cells.

106 ncing reproduced these functional effects on paracellular ion permeability.

107 Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney.

108 that pathogenic CLDN10 mutations affect TAL paracellular ion transport and cause a novel tight junct

109 ent specific selectivity and permeability of paracellular ion transport.

110 e to water in Ildr1 knockout animals whereas paracellular ionic permeabilities in the Ildr1 knockout

111 d lipoprotein receptor (LSR), a component of paracellular junctions at points in which three cell mem

112 n-5 paradoxically accompanies an increase in paracellular leak and rearrangement of alveolar tight ju

113 ripheral tolerance, and antigen delivered by paracellular leak initiates immune responses in the mese

114 , absorptive oxalate flux occurs through the paracellular "leak" pathway, and net absorption of dieta

115 We investigated whether transcytosis and paracellular leakage are co-regulated.

116 Importantly, inhibition of paracellular leakage by sphingosine-1-phosphate, which a

117 g transcytosis by dynamin blockade increased paracellular leakage concomitantly with the loss of cort

118 of transcytosis induced a rapid increase in paracellular leakage that was not explained by decreases

119 tinct transport pathways have been proposed: paracellular leakage through epithelial tight junctions

120 dies implicate occludin in the regulation of paracellular macromolecular flux at steady state and in

121 udin interactions are essential for limiting paracellular macromolecular flux.

122 t junction protein Claudin-10, show enhanced paracellular magnesium and calcium permeability and redu

123 bsorbed in the proximal tubule, primarily by paracellular mechanisms that are not sensitive to calciu

124 xtracellular form that uses transcellular or paracellular migration, or by infecting a host cell that

125 ni CCS treatment of BAT2 cells also enhanced paracellular migration.

126 as a static structure providing a barrier to paracellular movement and restricting proteins to the ap

127 -forming protein claudin-2 (CLDN-2) mediates paracellular Na(+) and water transport in leaky epitheli

128 ascending limb (TAL) of Henle's loop drives paracellular Na(+), Ca(2+), and Mg(2+) reabsorption via

129 l transmigration, either at the EC junction (paracellular) or directly through the EC body (transcell

130 Leakage can occur between (paracellular) or through (transcytosis) endothelial cell

131 tion of dietary oxalate results from passive paracellular oxalate absorption as modified by oxalate b

132 osinophils, mast cells (all, P < .0001), and paracellular passage (P = .02) were significantly higher

133 Claudin-21 also allows the paracellular passage of larger solutes.

134 ased intestinal permeability, which involves paracellular passage regulated through tight junctions (

135 NaPi-IIb/Slc34a2, and a poorly characterized paracellular passive pathway.

136 athway mostly mediated by NaPi-IIb while the paracellular pathway appears not to be affected.

137 The paracellular pathway could provide a route for passive H

138 lts suggest that HCO(3) (-) flux through the paracellular pathway counterbalances, in part, changes i

139 e claudin-14/16/19 proteins form a regulated paracellular pathway for calcium reabsorption, approache

140 or proinflammatory cytokines might alter the paracellular pathway function.

141 t function as both pores and barriers in the paracellular pathway in epithelial cells.

142 ndings have attested to the concept that the paracellular pathway is physiologically regulated throug

143 HCO(3) (-) flux through the paracellular pathway may counterbalance effects of cellu

144 at these features are mostly originated from paracellular pathway modifications due to host-parasite

145 nhibitors increased calcium reabsorption and paracellular pathway permeability but did not change NaC

146 rmeabilities of the basolateral membrane and paracellular pathway remain largely unknown.

147 rovascular endothelia (HMVEC-Ls) to open the paracellular pathway through Src family kinase (SFK) act

148 The paracellular pathway was pH-insensitive at pH 6.0 vs. pH

149 the flux of [(3)H]mannitol, a marker of the paracellular pathway, across intestine from wild-type an

150 cles disperse throughout the tissues via the paracellular pathway.

151 of claudin-14, the negative regulator of the paracellular pathway.

152 and ICAM-2 and occurred exclusively via the paracellular pathway.

153 rt depends strongly on the properties of the paracellular pathway.

154 sport in the TAL via the permeability of the paracellular pathway.

155 b/Slc34a2 and a poorly characterized passive/paracellular pathway.

156 epithelial transport across transcellular or paracellular pathways promises to advance the present un

157 iratory epithelia involves both cellular and paracellular pathways.

158 epithelia can occur via the transcellular or paracellular pathways.

159 bly of adherens junctions and opening of the paracellular pathways.

160 e data indicate that Pg bacteria may enhance paracellular penetration through oral mucosa in part by

161 Although the maximum temperature of paracellular penetration was similar for all four cell s

162 Paracellular permeabilities conferred by claudin-2 are c

163 Cl(-) and HCO(3) (-) had similar paracellular permeabilities in human airway epithelia.

164 ng PrP(c) knockdown; the cells had increased paracellular permeability (1.5-fold over 48 hours; P < .

165 sendothelial electrical resistance), reduced paracellular permeability (fluorescein isothiocyanate-de

166 l adhesion kinase mediates TGF-beta1-induced paracellular permeability and actin cytoskeleton dynamic

167 TGF-beta1 induces an increase in paracellular permeability and actin stress fiber formati

168 d by Claudin-1 absence, leading to increased paracellular permeability and liver injuries secondary t

169 Both paracellular permeability and the localization of TJ pro

170 mutation within ECs prevented VEGF-initiated paracellular permeability and tumor cell transmigration

171 Our findings indicate that transcytosis and paracellular permeability are co-regulated through a sig

172 ation, immunoblotting, immunohistochemistry, paracellular permeability assay, FACS, cytokine assay, a

173 SU6656 reduced TNF-alpha-mediated paracellular permeability changes, restored occludin, p1

174 We observed significant increase in paracellular permeability following siRNA-mediated suppr

175 resistance (TEER), indicating an increase of paracellular permeability for ions.

176 n-regulation of Sgpp2 attenuated LPS-induced paracellular permeability in cultured cells and enhanced

177 ion protein 1 (TJP1) gene, is a regulator of paracellular permeability in epithelia and endothelia.

178 Similarly, we observed an increase of paracellular permeability in NRC cells silenced for clau

179 Defect in claudin-1 expression increases paracellular permeability in polarized hepatic cell line

180 d to study cerebrovascular transcellular and paracellular permeability in vivo.

181 artially able to prevent the increase in BEC paracellular permeability induced by cytokines.

182 lts show that HMTBA prevents the increase in paracellular permeability induced by H2O2 or tumour necr

183 We show that murine paracellular permeability markedly decreases during post

184 We speculate that paracellular permeability may have evolved as a general

185 etween transcellular sodium reabsorption and paracellular permeability may prevent the backflow of re

186 cells, while the endocochlear potential and paracellular permeability of a biotin-based tracer in th

187 esistance was associated with an increase in paracellular permeability of glucose.

188 cofilin-1 by RNA interference increased the paracellular permeability of human colonic epithelial ce

189 tructural changes may selectively affect the paracellular permeability of ions or small molecules, re

190 ght junction membrane proteins that regulate paracellular permeability of renal epithelia to small io

191 Nutrient starvation reduced the paracellular permeability of small-sized urea but not la

192 ed TAL tubules of claudin-10-deficient mice, paracellular permeability of sodium is decreased, and th

193 This coincided with an increase of paracellular permeability of the BBB to the small tracer

194 tinal epithelium to dynamically regulate its paracellular permeability properties and better define t

195 as been demonstrated to transiently increase paracellular permeability properties to provide an addit

196 cture and function, although the increase of paracellular permeability returned to baseline after 24

197 tine tissues from PrP(c-/-) mice had greater paracellular permeability than from wild-type mice (105.

198 s cell polarity, cytoskeleton integrity, and paracellular permeability through inhibition of the smal

199 cing of Claudin-1 in Can 10 clones increased paracellular permeability to a level similar to that of

200 ased TEER (1.28- to 1.31-fold) and decreased paracellular permeability to FITC-Dextran, and this effe

201 sepithelial resistance, a marked decrease in paracellular permeability to fluorescence isothiocyanate

202 l TER, these monolayers do exhibit increased paracellular permeability to fluorescent dextrans.

203 ltured epithelial cells demonstrate enhanced paracellular permeability to large molecules, revealing

204 aired the development of TEER, and increased paracellular permeability to sodium fluorescein in airwa

205 abundance was associated with a reduction in paracellular permeability to sodium, whereas decreased c

206 t junction (TJ) has a key role in regulating paracellular permeability to water and solutes in the ki

207 port controls tight-junction composition and paracellular permeability via modulating expression of t

208 Paracellular permeability was assessed by fluorescein is

209 The role of autophagy in the modulation of paracellular permeability was confirmed by pharmacologic

210 lones, Claudin-1 was localized at the TJ and paracellular permeability was decreased, compared to par

211 Paracellular permeability was determined by quantifying

212 Paracellular permeability was measured by using fluoresc

213 Changes in barrier function and abnormal paracellular permeability were found in both interfollic

214 l barrier integrity and decreased intestinal paracellular permeability with a lower level of serum en

215 DRA-KO mice exhibited an increased colonic paracellular permeability with significantly decreased l

216 tent with the autophagy-induced reduction in paracellular permeability, a marked decrease in the leve

217 l cells in junction formation, regulation of paracellular permeability, and epithelial morphogenesis.

218 tercellular junctional distance, and induced paracellular permeability, loss of apico-basal polarity

219 luten-sensitized mice, P(HEMA-co-SS) reduced paracellular permeability, normalized anti-gliadin immun

220 role in regulating the maintenance of TJ and paracellular permeability, which may explain how various

221 and interferon-gamma significantly increased paracellular permeability, which was blocked by cotreatm

222 vated in the cecum of WD-fed mice, increased paracellular permeability, while the BA-binding resin se

223 ns at junctions, wound healing dynamics, and paracellular permeability.

224 ntal or mutant E. faecalis strains indicated paracellular permeability.

225 ansepithelial resistance (TER) and decreased paracellular permeability.

226 nce and reduced the ratio of sodium/chloride paracellular permeability.

227 d actin stress fiber formation and increased paracellular permeability.

228 ght junctions (TJs), structures that control paracellular permeability.

229 d actin stress fiber formation and prevented paracellular permeability.

230 s an important role in regulating epithelial paracellular permeability.

231 human microvascular endothelium and measured paracellular permeability.

232 tion of tight and adherens junctions and BEC paracellular permeability.

233 We studied the role of claudin-1 in hepatic paracellular permeability.

234 channel (ENaC) subunits and claudin-8 affect paracellular permeability.

235 histamine results in a transient increase in paracellular permeability.

236 audin-1) that critically regulate epithelial paracellular permeability.

237 sodium/hydrogen exchanger 3 (NHE3), reduces paracellular phosphate transport.

238 The paracellular pore appears to primarily be lined by polar

239 er function by activating claudin-2-mediated paracellular pore pathways.

240 into how ion selectivity is achieved in the paracellular pore.

241 (Cldn2), a tight junction protein that forms paracellular pores and increases urothelial permeability

242 extracellular loop (ECL1) of claudins forms paracellular pores in the tight junction that determine

243 and reversible, characteristic of a passive, paracellular process, and blocked by reduced temperature

244 transport in the distal intestine involves a paracellular process, we found that the 1,25-dihydroxyvi

245 Fc domain, consistent with FcRn-independent paracellular, rather than transcellular, transport of an

246 uring inflammatory TJ complex remodeling and paracellular route formation in brain endothelial cells.

247 of apparent permeability coefficient suggest paracellular route of transport of investigated compound

248 internalization via macropinocytosis during paracellular route opening.

249 lectric resistance (TEER) and opening of the paracellular route to 4kDa fluorescent dextran but not 7

250 non-toxic manner but transiently opened the paracellular route to both 4 and 70kDa fluorescent dextr

251 mechanisms in parallel to the well-described paracellular route to modulate solute transport from the

252 uman IEC, which occurred predominately via a paracellular route, was significantly associated with cl

253 nsulin suggested its uptake occurred via the paracellular route.

254 er also flow into the intestinal lumen via a paracellular route.

255 34a2-deficient mice, and analysed trans- vs. paracellular routes of phosphate absorption.

256 sodium reabsorption takes transcellular and paracellular routes.

257 to actin may allow for accommodation of the paracellular seal to physiological or pathological alter

258 is necessary for tight junction assembly and paracellular sealing in trophectoderm epithelium.

259 tive apical ion transport is balanced out by paracellular shunting of acid/base.

260 We show that claudin-10 determines paracellular sodium permeability, and that its loss lead

261 ubule (PT) of the kidney, claudin-2 mediates paracellular sodium reabsorption.

262 oltage is increased, leading to a shift from paracellular sodium transport to paracellular hyperabsor

263 tricellular tight junctions (tTJs) seal the paracellular space between epithelial cells.

264 a1 tightened the monolayer by decreasing the paracellular space between migrating epithelial cells.

265 lls that restricts solutes from crossing the paracellular space, creating a microenvironment within s

266 nnect adjacent epithelial cells and seal the paracellular space.

267 selectively permeable barriers that seal the paracellular space.

268 nd nutrients would be dissipated through the paracellular space.

269 menon: penetration of extracellular ice into paracellular spaces at the cell-cell interface.

270 ns (TJs), down-regulation of which may widen paracellular spaces between cells, allowing greater flui

271 ing perturbations in the permeability of the paracellular spaces between epithelial barriers.

272 ction of the movement of solutes through the paracellular spaces in the neurovascular unit is a key m

273 functioning as barrier and/or channel in the paracellular spaces of epithelia.

274 pport an increased movement of cells through paracellular spaces.

275 ith IFN-gamma induced endothelial leakage of paracellular tracers.

276 We conclude that DXR increases paracellular transit of small macromolecules, including

277 zed that DXR treatment resulted in increased paracellular translocation of bacteria or bacterial prod

278 scle, intravascular adherence and subsequent paracellular transmigration of neutrophils elicited by t

279 or PAF-elicited intravascular adherence and paracellular transmigration of neutrophils.

280 Paracellular transmigration predominates (>/=90% of even

281 il preference for the transcellular over the paracellular transmigration route.

282 E-cadherin cleavage, loss of cell adherence, paracellular transmigration, and basolateral invasion.

283 otes ICAM-1-mediated neutrophil crawling and paracellular transmigration.

284 ely induced EC barrier resistance, decreased paracellular transport and increased protein expression

285 , and the mechanisms by which CaSR regulates paracellular transport in the kidney remain unknown.

286 Our results indicate that paracellular transport in the PT is required for efficie

287 and a consequent about 3-fold improvement in paracellular transport of insulin.

288 eptors, integrins, play a role in regulating paracellular transport of renal proximal tubule cells.

289 zed iron oxide nanoparticles, activating the paracellular transport pathway and facilitating the loca

290 portance of transcellular (vesicular) versus paracellular transport pathways by LECs and how mechanic

291 of tight and adherens junctions that define paracellular transport properties of terminally differen

292 maintaining epithelial polarity, regulating paracellular transport, and providing barrier function.

293 roximal tubule allows both transcellular and paracellular transport, while the collecting duct primar

294 ude wider than what is normally reported for paracellular transport.

295 uctural and functional components regulating paracellular transport.

296 ited to small molecules, as expected for the paracellular water and Na(+) channel formed by claudin-2

297 Vasopressin cannot correct paracellular water loss in Ildr1 knockout animals despit

298 xpression of Ildr1 significantly reduces the paracellular water permeability.

299 tricellular tight junction is important for paracellular water permeation and that Ig-like domain co

300 -2 is a tight junction protein that mediates paracellular water transport in intestinal epithelia, re