ライフサイエンスコーパス: BMEC

1 BMEC were cultured and identified by electron microscopy

2 BMEC-1 monolayers were grown to confluency on 3 microns

3 BMECs co-expressing SV40T, hTERT and N-ras exhibited an

4 BMECs derived from human iPSCs in SZ and BD did not show

5 BMECs from the BBB-deficit group show increased matrix m

6 BMECs transfected with hTERT alone were functionally and

7 BMECs transfected with SV40T (BMSVTs) had an extended li

8 BMECs were isolated from milk and treated with various l

9 BMECs were isolated from rats of different ages (10 days

10 the passage of citalopram enantiomers across BMEC monolayers was not stereoselective.

11 also did not enhance Tx-67 permeation across BMEC monolayers.

12 The transport across BMEC monolayers was polarized for both Tx-67 and Taxol w

13 t modify the permeation of citalopram across BMECs.

14 t suggesting that passage of the drug across BMECs was mediated by a carrier mechanism.

15 ates coated with interleukin-1beta-activated BMEC.

16 nces in the capacities of neonatal and adult BMECs to interact with E. coli.

17 sion capacities of newborn compared to adult BMECs.

18 These findings suggest that CRF could affect BMEC structure or function, as reported for increased cA

19 For MREH and BMEC, the CO(2)EM was 73.4 metric tons annually (if all

20 UHCW and BMEC utilized single-use 30 mL and 75 mL cannisters, res

21 rming cells [GM-CFCs] adhering to HUVECs and BMECs, respectively), but were unable to migrate to any

22 0.6% of GM-CFCs migrating across HUVECs and BMECs, respectively).

23 3.1% of GM-CFCs migrating across HUVECs and BMECs, respectively; P < .01, n = 6).

24 nt of PSA in the interactions between PC and BMECs, we performed a cell-cell adhesion assay.

25 nal extracellular domains of OmpA as well as BMEC receptor analogues for OmpA, chitooligomers (GlcNAc

26 rresponded to elevated HA synthesis and avid BMEC adhesion.

27 Complete understanding of bacteria-BMEC interactions contributing to translocation of the B

28 Immunoprecipitation of biotinylated BMEC membrane proteins and immunocytochemistry studies o

29 creased membrane integrin activation in both BMEC and HSC/P, and in HSC/P de-adhesion and mobilizatio

30 ng molecule/receptor (Ibe10R) on both bovine BMEC (HBMEC) and human BMEC (HBMEC) that is responsible

31 immunoblotting and were purified from bovine BMEC by wheat germ agglutinin and Maackia amurensis lect

32 in homeostatic murine BMECs (MBMECs), bovine BMECs (BBMECs), and porcine BMECs (PBMECs) and pinpointe

33 how metastatic prostate cancer cells breach BMEC monolayers in a step-wise fashion under physiologic

34 The expression and secretion of eCyPA by BMECs was enhanced by BCL9, a Wnt-beta-catenin transcrip

35 bstantially enhanced rhodamine 123 uptake by BMECs through inhibition of Pgp.

36 . coli-brain microvascular endothelial cell (BMEC) interactions contributing to E. coli traversal of

37 itro using two bone marrow endothelial cell (BMEC) lines and four prostate adenocarcinoma cell lines

38 (PC3M-LN4) to bone marrow endothelial cell (BMEC) lines requires a pericellular hyaluronan (HA) matr

39 m into brain microvascular endothelial cell (BMEC)-like cells as in vitro model of the BBB.

40 lls to brain microvascular endothelial cell (BMEC)-like cells with good barrier properties and mature

41 whether these discrete prostate cancer cell-BMEC adhesive contacts culminate in cooperative, step-wi

42 human brain microvascular endothelial cells (BMEC) and EA.hy 926, a human umbilical vein endothelial

43 and actin in bone marrow endothelial cells (BMEC) and HSC/P, which results in decreased membrane int

44 human brain microvascular endothelial cells (BMEC) and its role as a stimulus for endothelial cell ac

45 is of brain microvascular endothelial cells (BMEC) by E. coli within an endosome to avoid lysosomal f

46 y the role of bone marrow endothelial cells (BMEC) in the regulation of hematopoietic cell traffickin

47 nvade brain microvascular endothelial cells (BMEC) in vitro and to cross the blood-brain barrier in v

48 on of brain microvascular endothelial cells (BMEC) is a prerequisite for successful crossing of the b

49 tion on brain microvessel endothelial cells (BMEC) isolated from rat and bovine brain.

50 with brain microvascular endothelial cells (BMEC) significantly more than with fibroblasts or arachn

51 f the brain microvascular endothelial cells (BMEC) that constitute the blood-brain barrier both in vi

52 binds brain microvascular endothelial cells (BMEC) via a lectin-like activity of SfaS adhesin specifi

53 itro, brain microvascular endothelial cells (BMEC) were incubated with K1(+) and K1(-) E. coli strain

54 grate through bone marrow endothelial cells (BMEC), and release platelets within the sinusoidal space

55 nvade brain microvascular endothelial cells (BMEC), for example growth in media supplemented with 50%

56 on of brain microvascular endothelial cells (BMEC), host cell actin cytoskeleton rearrangements and r

57 ithin brain microvascular endothelial cells (BMEC), the principal cell layer composing the blood-brai

58 human brain microvascular endothelial cells (BMEC), the single-cell layer which constitutes the blood

59 imary brain microvascular endothelial cells (BMEC), we demonstrate that the vascular endothelial grow

60 nt of brain microvascular endothelial cells (BMEC), which constitute a lining of the blood-brain barr

61 human brain microvascular endothelial cells (BMEC), which constitute the blood-brain barrier.

62 ng of brain microvascular endothelial cells (BMEC).

63 human brain microvascular endothelial cells (BMEC).

64 nvade brain microvascular endothelial cells (BMEC).

65 er of brain microvascular endothelial cells (BMEC).

66 human brain microvascular endothelial cells (BMEC).

67 ts of brain microvascular endothelial cells (BMEC).

68 on of brain microvascular endothelial cells (BMEC).

69 er of brain microvascular endothelial cells (BMEC).

70 arriers and human brain microvascular cells (BMEC), a human blood-brain barrier model, were studied.

71 uring brain microvascular endothelial cells (BMECs) and human mesenchymal stem cells (MSCs).

72 ts of brain microvascular endothelial cells (BMECs) and pericytes, which share a basement membrane an

73 mouse brain microvascular endothelial cells (BMECs) changes expression of multiple genes involved in

74 lly adhere to bone marrow endothelial cells (BMECs) compared with endothelial linings from other tiss

75 Bone marrow endothelial cells (BMECs) form a network of blood vessels that regulate bot

76 123 by brain microvessel endothelial cells (BMECs) in the presence of the agent.

77 on of brain microvascular endothelial cells (BMECs) is a key step in the pathogenesis of meningitis d

78 on of brain microvascular endothelial cells (BMECs) is a prerequisite for penetration into the centra

79 that aging of bone marrow endothelial cells (BMECs) leads to an altered crosstalk between the BMEC ni

80 ic to brain microvascular endothelial cells (BMECs) or arise via effects of peripheral inflammatory c

81 Bone marrow endothelial cells (BMECs) play a key role in bone formation and haematopoie

82 th sinusoidal bone marrow endothelial cells (BMECs) promote thrombopoietin (TPO)-independent platelet

83 human brain microvascular endothelial cells (BMECs) than the parent strain.

84 f the brain microvascular endothelial cells (BMECs) that comprise the BBB.

85 es of brain microvascular endothelial cells (BMECs) were analyzed as markers of angiogenesis.

86 mouse brain microvascular endothelial cells (BMECs) were cultured and treated with Malat1 GapmeR befo

87 on of brain microvascular endothelial cells (BMECs) with the chemokine CCL2 (formerly called MCP-1).

88 human brain microvascular endothelial cells (BMECs), a human blood-brain barrier (BBB) model system,

89 r secreted by bone marrow endothelial cells (BMECs), is critical to MM homing, progression, survival,

90 ising brain microvascular endothelial cells (BMECs), pericytes, astrocytes and neurons derived from r

91 , secreted by bone marrow endothelial cells (BMECs), promoted the colonization and proliferation of M

92 to bone marrow sinusoidal endothelial cells (BMECs), stimulating thrombopoiesis.

93 rough brain microvascular endothelial cells (BMECs), which compose the blood-brain barrier (BBB).

94 bovine brain microvessel endothelial cells (BMECs).

95 tegy to study bone marrow endothelial cells (BMECs).

96 imary brain microvascular endothelial cells (BMECs).

97 4-2B cells to bone marrow endothelial cells (BMECs).

98 ly by brain microvascular endothelial cells (BMECs).

99 Brain microvascular endothelial-like cells (BMECs) differentiated from human-derived induced pluripo

100 MREH) and Birmingham and Midland Eye Centre (BMEC) (the second and third largest VR centers in the UK

101 In conclusion, BMEC-1 cells support transmigration of hematopoietic pro

102 Western blot analysis of cultured BMEC identified CRF receptor protein; stimulation with C

103 induced pluripotent stem cell (iPSC)-derived BMEC-like cells as a model BBB substrate on which to min

104 Human iPSC-derived BMEC-like cells are thus suitable to explore the molecul

105 Also, MS-derived BMEC-like cells displayed an inflammatory phenotype with

106 MS-derived BMEC-like cells showed impaired junctional integrity, ba

107 n human pluripotent stem cell (hPSC)-derived BMECs, particularly through adherens junction, tight jun

108 RA-treated hPSC-derived BMECs were subsequently co-cultured with primary human b

109 iPSC-derived BMECs display a strong barrier phenotype, express key vi

110 We paired iPSC-derived BMECs with recombinant vitamin A serum transport protein

111 zation, and transcytosis across iPSC-derived BMECs.

112 Endomucin expression discriminates BMECs in populations exhibiting mutually exclusive prope

113 t in cultured murine brain microvascular EC (BMEC) monolayers, but interleukin-1beta and tumor necros

114 f three cultures of bone marrow-derived ECs (BMECs).

115 Importantly, EECM-BMEC-like cells exhibited constitutive cell surface expr

116 Co-culture of EECM-BMEC-like cells with hiPSC-derived smooth muscle-like ce

117 as confirmed by T-cell interaction with EECM-BMEC-like cells.

118 esion molecules expressed on BM endothelium (BMEC) and chemokine stromal derived factor-1 (SDF-1).

119 nt cells across the bone marrow endothelium (BMEC) remains a poorly understood step in metastasis.

120 y greater for the growth condition enhancing BMEC invasion (50% NBS) than for the condition repressin

121 We examined BMEC function using stem cell-based models to identify c

122 f BMEC by increasing the affinity of MKs for BMEC.

123 of E. coli to invade BMECs were similar for BMECs derived from young and old rats and from human fet

124 t with a model in which HA matrix formation, BMEC adhesion, and metastatic potential are mediated by

125 BBB integrity or permeability compared to HC BMECs.

126 However, it is not clear how BMECs balance these dual roles, and whether these events

127 cific for NeuAc alpha2,3-galactose; however, BMEC molecules bearing these epitopes have not been iden

128 studies, we have taken advantage of a human BMEC-derived cell line (BMEC-1), which proliferates inde

129 ly, traversal of B. burgdorferi across human BMEC induces the expression of plasminogen activators, p

130 adhere, invade, and transcytose across human BMEC without affecting monolayer integrity.

131 be10R) on both bovine BMEC (HBMEC) and human BMEC (HBMEC) that is responsible for invasion by E. coli

132 cytose to the basal surface of rat and human BMEC in a manner dependent on the PAF receptor and the p

133 n neutrophils, murine macrophages, and human BMEC, which was linked to increased susceptibility to ki

134 d that B. burgdorferi appeared to bind human BMEC by their tips near or at cell borders, suggesting a

135 B. burgdorferi differentially crosses human BMEC and HUVEC and that the human BMEC form a barrier to

136 man LCM microvessel data with existing human BMEC transcriptomic datasets, we identified novel putati

137 1, there was a significant decrease in human BMEC (HBMEC) invasion.

138 to bud and develop pseudohyphae inside human BMEC without apparent morphological changes of the host

139 Invasion of C. albicans into human BMEC was demonstrated by using an enzyme-linked immunoso

140 isiae were not able to bind and invade human BMEC.

141 we showed that OmpA binds to a 95-kDa human BMEC (HBMEC) glycoprotein (Ecgp) for E. coli invasion.

142 show here that E. coli K1 infection of human BMEC (HBMEC) results in activation of caveolin-1 for bac

143 kinase (FAK) in E. coli K1 invasion of human BMEC (HBMEC).

144 ay a major role in E. coli invasion of human BMEC (HBMEC).

145 how that attachment to and invasion of human BMEC by B. anthracis Sterne is mediated by the pXO1 plas

146 EC, e.g., pseudopod-like structures on human BMEC membrane and intracellular vacuole-like structures

147 sses human BMEC and HUVEC and that the human BMEC form a barrier to traversal.

148 dition, C. albicans penetrates through human BMEC monolayers without a detectable change in transendo

149 Binding of C. albicans to human BMEC was time and inoculum dependent.

150 Both in vitro (human BMEC) (HBMEC) and in vivo (mice) models of BBB were used

151 the interaction(s) of C. albicans with human BMEC should contribute to the understanding of the patho

152 dies revealed that on association with human BMEC, C. albicans formed germ tubes and was able to bud

153 tages of C. albicans interactions with human BMEC, e.g., pseudopod-like structures on human BMEC memb

154 found that T. b. gambiense crossing of human BMECs was abrogated by N-methylpiperazine-urea-Phe-homop

155 etastatic prostate tumor cells roll on human BMECs under physiological flow conditions.

156 pathogenic effects in vitro on primary human BMECs (HBMECs).

157 enhance amyloid-beta (Abeta) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (al

158 E. coli induced the accumulation of actin in BMEC to a level similar to that induced by the parental

159 These results show potential deficits in BMEC-like cells in psychotic disorders that result in BB

160 cytoskeletal rearrangements are essential in BMEC invasion by E. coli K1 and L. monocytogenes, the un

161 significantly increased basal NO release in BMEC.

162 ive ability of the parent strain in vitro in BMEC and was significantly less invasive in the central

163 induced cell death and Caspase 3 activity in BMECs.

164 monstrate that our strategy inhibits CyPA in BMECs, preventing MM cell extravasation in vitro.

165 d tube formation properties were enhanced in BMECs from diabetic rats, which also expressed high leve

166 gambiense failed to elicit calcium fluxes in BMECs, suggesting that generation of activation signals

167 reased VEGF-dependent angiogenic function in BMECs is mediated by peroxynitrite and involves c-src an

168 adhesion in the cytokine-induced pathway in BMECs in the context of other cytokine-inducible endothe

169 the level of the parent E. coli K1 strain in BMECs with constitutively active RhoA.

170 ins, VE-cadherin and beta-catenin, increased BMEC paracellular permeability, and facilitated the abil

171 ith 50% newborn bovine serum (NBS) increased BMEC invasion, whereas growth in media supplemented with

172 hermore, VEGF and NO significantly increased BMEC migration, which was mediated by the up-regulation

173 echanism for neutrophil adhesion to infected BMEC under static conditions.

174 Binding and invasion of intact BMEC monolayers were independent of the L. monocytogenes

175 complementation with the OmpA+ E. coli into BMEC.

176 ntrol (HC) subjects were differentiated into BMEC-"like" cells.

177 s exhibited binding and internalization into BMECs as well as binding to both human and mouse BBB in

178 deletion mutant (IB7D5) was unable to invade BMEC.

179 Also, the abilities of E. coli to invade BMECs were similar for BMECs derived from young and old

180 nt for the majority of CNS isolates, invaded BMEC more efficiently than strains from other common GBS

181 The 65-kDa BMEC glycoprotein showed effective inhibition of S fimbr

182 Mean CO(2)EM per patient was: MREH 111.8 kg, BMEC 7.5 kg, and UHCW 2.7 kg.

183 n contrast to arterial-like, sinusoidal-like BMECs are short-lived, form 2D-networks, contribute to i

184 y and expansion and preserve sinusoidal-like BMECs ex vivo.

185 advantage of a human BMEC-derived cell line (BMEC-1), which proliferates independent of growth factor

186 ) isolated from lungs (LECs) or bone marrow (BMECs) of young (3-4 months) and old (22-24 months), mal

187 Maximal BMEC adhesion and HA encapsulation were associated with

188 ells and cultured bone marrow microvascular (BMECs) and human umbilical vein endothelial cells (HUVEC

189 d Malat1 levels were found in cultured mouse BMECs after OGD as well as in isolated cerebral microves

190 ust expression of S1P4 in homeostatic murine BMECs (MBMECs), bovine BMECs (BBMECs), and porcine BMECs

191 the Ibe10 of E. coli interacts with a novel BMEC surface protein, Ibe10R, for invasion of both BBMEC

192 with an optimized seeding condition of NSCs, BMECs and MSCs.

193 Activation of BMEC with interleukin 1beta resulted in a threefold incr

194 eractions are dependent on the expression of BMEC E-selectin and sialylated glycoconjugates on bone-m

195 microvessels, implicating the importance of BMEC adhesion in the predilection of prostate tumor meta

196 Central to E. coli internalization of BMEC is the expression of OmpA (outer membrane protein A

197 h conditions enhanced E. coli K1 invasion of BMEC 3- to 10-fold: microaerophilic growth, media buffer

198 erminants that contribute to the invasion of BMEC have been identified, little is known about the GBS

199 These data suggest that invasion of BMEC is a mechanism for triggering inflammation and leuk

200 GBS invasion of BMEC may be a primary step in the pathogenesis of mening

201 GBS invasion of BMEC monolayers was demonstrated by electron microscopy.

202 GBS invasion of BMEC required active bacterial DNA, RNA, and protein syn

203 At high bacterial densities, GBS invasion of BMEC was accompanied by evidence of cellular injury; thi

204 GBS invasion of BMEC was quantified with a gentamicin protection assay.

205 re identified to enhance E. coli invasion of BMEC, an important event in the pathogenesis of E. coli

206 gene was involved in E. coli K1 invasion of BMEC, i.e., the invasive ability of E. coli K1 was signi

207 Cytochalasin D abrogated invasion of BMEC, whereas genistein effected only a 53% decrease in

208 lin A completely blocked E. coli invasion of BMEC.

209 ibeB is required for E. coli K1 invasion of BMEC.

210 gnificantly enhances the E. coli invasion of BMEC.

211 omplemented the TnphoA mutant in invasion of BMEC.

212 sis-like endocytic mechanism for invasion of BMEC.

213 OmpA domains involved in E. coli invasion of BMEC.

214 ic oxide (NO), resulting in the migration of BMEC.

215 critical step in CCL2-induced modulation of BMEC junctional protein expression and integrity, and po

216 s to migrate through confluent monolayers of BMEC by increasing the affinity of MKs for BMEC.

217 was completely eliminated by pretreatment of BMEC with proteinase K.

218 proteins and immunocytochemistry studies of BMEC with anti-S fimbria-binding protein antibodies reve

219 was increased by cycloheximide treatment of BMEC (P = 0.0059) but was not affected by nitric oxide s

220 may contribute to a better understanding of BMEC angiogenesis and the physiological as well as patho

221 RNA sequencing and qPCR analysis of BMECs suggested the involvement of S1P4 in endothelial h

222 s in the bone marrow (BM), the complexity of BMECs is not fully characterized.

223 ese data improve the molecular definition of BMECs and brain pericytes, and are a resource for ration

224 ncing, we defined a spatial heterogeneity of BMECs and identified a capillary subtype, termed type S

225 cPLA2) contributes to E. coli K1 invasion of BMECs but not to L. monocytogenes invasion of BMECs.

226 ivity (50 times) in blocking the invasion of BMECs by Escherichia coli K1 than did the partial protei

227 , we demonstrate that E. coli K1 invasion of BMECs requires RhoA activation.

228 t CNF1 contributes to E. coli K1 invasion of BMECs.

229 rtant determinant for E. coli K1 invasion of BMECs.

230 MECs but not to L. monocytogenes invasion of BMECs.

231 significantly inhibit E. coli K1 invasion of BMECs.

232 Apical S1P treatment of BMECs tightened the endothelial barrier in vitro, wherea

233 ut improved migration characteristics in old BMECs.

234 is causally linked to the action of CCL2 on BMEC junctional protein expression and barrier integrity

235 ns reacted to 65-kDa protein present only on BMEC, not on systemic vascular endothelial cells.

236 Prostate cancer cells tethered and rolled on BMEC and then firmly adhered to and traversed BMEC via s

237 endothelium, is constitutively expressed on BMECs, suggesting that prostate tumor cells could use th

238 monstrated transcytosis across intact, polar BMEC monolayers grown on Transwell membranes.

239 (MBMECs), bovine BMECs (BBMECs), and porcine BMECs (PBMECs) and pinpointed its localization to ablumi

240 helial growth factor signaling and preserves BMEC tight junctions.

241 Single-cell mRNA sequencing of primary BMECs reveals that their diversity and native molecular

242 ctively) are abundantly expressed on primary BMECs and promote HIV-1 attachment and entry.

243 n adhesion of E. coli to cow, human, and rat BMEC but did not enhance E. coli adhesion to systemic va

244 The bindings of E. coli to young and old rat BMECs were similar.

245 Heat killing significantly reduced BMEC crossing but not binding.

246 Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions unde

247 sion in these cells was examined by studying BMECs derived from wild-type mice and P-selectin-deficie

248 Macrophages sustain BMEC cellular diversity and expansion and preserve sinus

249 Other experiments showed that BMEC infection stimulated monocyte and neutrophil adhesi

250 Given that BMECs lack the entry receptor CD4, HIV-1 must use recept

251 s) leads to an altered crosstalk between the BMEC niche and HSPCs, which instructs young HSPCs to beh

252 constitutive expression of E-selectin by the BMEC in vivo, we have found that vascular endothelial gr

253 ctin that is constitutively expressed by the BMEC in vivo.

254 elet-activating factor (PAF) receptor on the BMEC.

255 7-7B was capable of completely restoring the BMEC invasion of the noninvasive TnphoA mutant 7A-33 and

256 of the cells that transmigrated through the BMEC monolayers in response to SDF-1 demonstrated the pr

257 ripheral blood CD34+ cells were added to the BMEC-1 monolayer in the upper chamber of the 6-well plat

258 ting Ang-II production or signalling through BMEC AT2R, HSCP Ang-II receptor type 1 (AT1R)/AT2R or HS

259 icroscopy that E. coli transmigrates through BMEC in an enclosed vacuole without intracellular multip

260 ely deliver caveolin-1 siRNA (Ad-siCav-1) to BMEC monolayers, which model the blood-brain barrier (BB

261 adhere rapidly and specifically (70-90%) to BMEC-1 and trHBMEC bone marrow endothelial cells, but no

262 ostate cancer cells exhibit firm adhesion to BMEC via beta1, beta4, and alphaVbeta3 integrins in stat

263 Specific adhesion to BMEC-1 and trHBMEC was dependent upon the presence of a

264 of S fimbria-mediated binding of E. coli to BMEC.

265 ed in the binding of S-fimbriated E. coli to BMEC.

266 proteins, AslA, TraJ, and CNF1 contribute to BMEC invasion.

267 and expresses adhesion molecules similar to BMEC in vivo.

268 ells retained pericellular HA and adhered to BMECs.

269 tate tumor cell HA production on adhesion to BMECs.

270 NA (siRNA) diminished C4-2B cell adhesion to BMECs.

271 odies to PSA attenuated PC cells adhesion to BMECs.

272 o not assemble a HA matrix, adhere poorly to BMECs, and express normal levels of HAS.

273 Adhesion of these transfectants to BMECs was significantly diminished, comparable to the lo

274 One hTERT transduced BMEC culture underwent a long proliferative lag before r

275 MEC and then firmly adhered to and traversed BMEC via sequential dependence on E-selectin ligands and

276 Furthermore, treating BMECs with cavtratin, a synthetic cell-permeable peptide

277 Two BMEC-binding molecules for S fimbriae were identified as

278 Using transwell chambers with BMEC barriers, we found that serotype 1 crossed into the

279 tive cPLA2 inhibitor, and was confirmed with BMEC derived from cPLA2 knockout mice.

280 esting that cellular interaction of MKs with BMEC is critical for the migration of MKs.

281 othesis, we developed an in vitro model with BMEC isolated from a human, immortalized by simian virus

282 capable of intracellular replication within BMEC.

283 GBS survived within BMEC for up to 20 h without significant intracellular re

284 leads to a decrease in mTOR signaling within BMECs that potentially underlies the age-related impairm