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 transfected with hTERT alone were functionally and

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

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

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

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

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

10 t modify the permeation of citalopram across BMECs.

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

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

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

14 sion capacities of newborn compared to adult BMECs.

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

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

17 0.6% of GM-CFCs migrating across HUVECs and BMECs, respectively).

18 3.1% of GM-CFCs migrating across HUVECs and BMECs, respectively; P < .01, n = 6).

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

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

21 rresponded to elevated HA synthesis and avid BMEC adhesion.

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

23 Immunoprecipitation of biotinylated BMEC membrane proteins and immunocytochemistry studies o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 human brain microvascular endothelial cells (BMEC).

55 nvade brain microvascular endothelial cells (BMEC).

56 er of brain microvascular endothelial cells (BMEC).

57 human brain microvascular endothelial cells (BMEC).

58 on of brain microvascular endothelial cells (BMEC).

59 er of brain microvascular endothelial cells (BMEC).

60 ts of brain microvascular endothelial cells (BMEC).

61 ng of brain microvascular endothelial cells (BMEC).

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

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

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

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

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

67 123 by brain microvessel endothelial cells (BMECs) in the presence of the agent.

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

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

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

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

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

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

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

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

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

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

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

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

80 bovine brain microvessel endothelial cells (BMECs).

81 4-2B cells to bone marrow endothelial cells (BMECs).

82 ly by brain microvascular endothelial cells (BMECs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 1, there was a significant decrease in human BMEC (HBMEC) invasion.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 significantly increased basal NO release in BMEC.

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

130 induced cell death and Caspase 3 activity in BMECs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Maximal BMEC adhesion and HA encapsulation were associated with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 gnificantly enhances the E. coli invasion of BMEC.

170 omplemented the TnphoA mutant in invasion of BMEC.

171 sis-like endocytic mechanism for invasion of BMEC.

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

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

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

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

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

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

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

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

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

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

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

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

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

185 significantly inhibit E. coli K1 invasion of BMECs.

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

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

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

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

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

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

192 helial growth factor signaling and preserves BMEC tight junctions.

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

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

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

196 Heat killing significantly reduced BMEC crossing but not binding.

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

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

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

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

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

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

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

204 7-7B was capable of completely restoring the BMEC invasion of the noninvasive TnphoA mutant 7A-33 and

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

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

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

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

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

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

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

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

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

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

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

216 and expresses adhesion molecules similar to BMEC in vivo.

217 ells retained pericellular HA and adhered to BMECs.

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

219 odies to PSA attenuated PC cells adhesion to BMECs.

220 tate tumor cell HA production on adhesion to BMECs.

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

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

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

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

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

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

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

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

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

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

231 capable of intracellular replication within BMEC.

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