ライフサイエンスコーパス: gastric epithelial cell

1 n internalization and barrier dysfunction in gastric epithelial cells.

2 totic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells.

3 transporter that is abundantly expressed in gastric epithelial cells.

4 CagA directly through the plasma membrane of gastric epithelial cells.

5 ndritic cells, macrophages, fibroblasts, and gastric epithelial cells.

6 lpAB reduced interleukin (IL)-6 induction in gastric epithelial cells.

7 secretion system that translocates CagA into gastric epithelial cells.

8 gene expression in H. pylori-infected human gastric epithelial cells.

9 against acid injury and oxidative stress in gastric epithelial cells.

10 nd increases the expression of IL-8 in human gastric epithelial cells.

11 iously shown that H. pylori binds to CD74 on gastric epithelial cells.

12 the capacity to induce interleukin (IL)8 in gastric epithelial cells.

13 ), which was found to be highly expressed by gastric epithelial cells.

14 histo-blood group antigen on the surface of gastric epithelial cells.

15 by inducing apoptosis and DNA damage in host gastric epithelial cells.

16 ioxidants on APE-1/Ref-1 expression in human gastric epithelial cells.

17 n and messenger RNA were detected in resting gastric epithelial cells.

18 nt to the site of bacterial adhesion on host gastric epithelial cells.

19 hanges in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells.

20 overexpression in neoplastic but not normal gastric epithelial cells.

21 of a low level reservoir of H. pylori within gastric epithelial cells.

22 could regulate the response to H. pylori in gastric epithelial cells.

23 /2 phosphorylation in H. pylori-infected AGS gastric epithelial cells.

24 ri to induce NF-kappaB-mediated apoptosis in gastric epithelial cells.

25 amma modified H. pylori-induced apoptosis in gastric epithelial cells.

26 of H. pylori on mucin synthesis in cultured gastric epithelial cells.

27 d in the basolateral membrane and cytosol of gastric epithelial cells.

28 monoamine transporter 2 (VMAT2) promoter in gastric epithelial cells.

29 ensatory hyperproliferation by nonneoplastic gastric epithelial cells.

30 s mitogen-activated protein (MAP) kinases in gastric epithelial cells.

31 of an IL-8 cytokine inflammatory response in gastric epithelial cells.

32 changes that lead to genetic instability in gastric epithelial cells.

33 ynthesis of proinflammatory cytokine IL-8 in gastric epithelial cells.

34 ria as well as the induction of apoptosis in gastric epithelial cells.

35 ivity, which elevates IL-8 expression in AGS gastric epithelial cells.

36 om H. pylori-infected AGS and Kato III human gastric epithelial cells.

37 uced through urease activity may be toxic to gastric epithelial cells.

38 alpha-stimulated expression of IL8 in canine gastric epithelial cells.

39 isolates was analyzed during coculture with gastric epithelial cells.

40 ts monolayer permeability of polarized human gastric epithelial cells.

41 a cytotoxin generated by H pylori that kills gastric epithelial cells.

42 of HDM2 and subsequent degradation of p53 in gastric epithelial cells.

43 nfluence interleukin 8 secretion by the host gastric epithelial cells.

44 e biological consequences of these events in gastric epithelial cells.

45 ri, vacA, induces cytoplasmic vacuolation in gastric epithelial cells.

46 teinase-dependent release of EGFR ligands in gastric epithelial cells.

47 ori-infected patients and in vitro using AGS gastric epithelial cells.

48 triggers activation of the COX-2 gene in rat gastric epithelial cells: action mediated through the ER

49 Ca(2+) selectively increases in restituting gastric epithelial cells adjacent to the damaged cells.

50 s and dendritic cells, as well as from human gastric epithelial cells (AGS cell line).

51 MKN45 gastric epithelial cells, AGS cells, and human primary g

52 uce gastric injury by mediating adherence to gastric epithelial cells and by modulating proinflammato

53 nd chemoreceptor mutants adhered to cultured gastric epithelial cells and caused cellular release of

54 . pylori both increased apoptosis in primary gastric epithelial cells and decreased phagocytosis of t

55 The cagA gene product CagA is injected into gastric epithelial cells and disturbs cellular functions

56 er pylori translocates the protein CagA into gastric epithelial cells and has been linked to peptic u

57 synthesis and nuclear accumulation in human gastric epithelial cells and implicate APE-1/Ref-1 in th

58 n on the DNA damage response sensor, ATM, in gastric epithelial cells and in biopsy specimens from pa

59 lobal DNA methylation both in the dysplastic gastric epithelial cells and in gastric stromal myofibro

60 n contrast, hBD-2 expression is regulated in gastric epithelial cells and increases in response to in

61 contrast to the spiral form, binds poorly to gastric epithelial cells and induces little, if any, int

62 H. pylori binds to class II MHC molecules on gastric epithelial cells and induces their apoptosis.

63 ction by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through

64 t impaired in its ability to deliver CagA to gastric epithelial cells and initiate cell elongation.

65 er that is active in a rare subpopulation of gastric epithelial cells and investigated whether these

66 osal biopsy specimens as well as in isolated gastric epithelial cells and lamina propria mononuclear

67 Primary gastric epithelial cells and MKN28 cells were cocultured

68 , how NO and H. pylori interact to signal in gastric epithelial cells and modulate the innate immune

69 Prolonged exposure of human gastric epithelial cells and mouse gastric cells to VacA

70 ted the effect of VacA on autophagy in human gastric epithelial cells and primary gastric cells from

71 airpin RNA (shRNA) libraries in AZ-521 human gastric epithelial cells and selected for VacA-resistant

72 Helicobacter pylori adheres to gastric epithelial cells and stimulates interleukin (IL)

73 an stomach by causing programmed necrosis of gastric epithelial cells and subsequent release of proin

74 e factor that causes multiple alterations in gastric epithelial cells and T cells.

75 i secretes a toxin, VacA, that targets human gastric epithelial cells and T lymphocytes and enhances

76 cyte-macrophage colony-stimulating factor by gastric epithelial cells and that these molecules induce

77 We investigated how cgt affects gastric epithelial cells and the host immune response.

78 We also investigated IL-18 levels in gastric epithelial cells and the monocyte cell line THP-

79 To address the fate of apoptotic gastric epithelial cells and their role in H. pylori muc

80 f cgt reduces cholesterol levels in infected gastric epithelial cells and thereby blocks IFNG signali

81 ndin synthesizing enzyme, cyclooxygenase) in gastric epithelial cells and whether this action is medi

82 ion is disrupted in elf+/- / Smad4+/- mutant gastric epithelial cells, and could be rescued by ectopi

83 levels of SMO, apoptosis, and DNA damage in gastric epithelial cells, and knockdown or inhibition of

84 lized at the interface between H. pylori and gastric epithelial cells, and previous studies suggested

85 determine the function of these molecules on gastric epithelial cells, antibodies to B7-1 and B7-2 we

86 clooxygenase may perturb the balance between gastric epithelial cell apoptosis (ulcer formation) and

87 These results indicate that VacA induces gastric epithelial cell apoptosis and suggest that diffe

88 hesis that there is a relative deficiency of gastric epithelial cell apoptosis associated with the ca

89 H pylori infection stimulated gastric epithelial cell apoptosis in EGFRwa2 but not in

90 H. pylori vacuolating toxin (VacA) to induce gastric epithelial cell apoptosis.

91 Other gastric epithelial cells appeared normal.

92 disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed af

93 the current study, we show that AZ-521 human gastric epithelial cells are highly susceptible to VacA-

94 Since human gastric epithelial cells are readily available from dono

95 critical role of the 3'SL structure on human gastric epithelial cells as an adherence ligand for rece

96 expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohis

97 Infection of gastric epithelial cells by H. pylori triggers an autocr

98 Knockdown of Muc1 expression in AGS human gastric epithelial cells by RNA interference was associa

99 pylori directly contributes to the injury of gastric epithelial cells by the elaboration of cytotoxic

100 NF-kappa B activation was decreased in MKN45 gastric epithelial cells by transfection of dominant-neg

101 y activates ERK, p38, and JNK MAP kinases in gastric epithelial cells; cag+ isolates are more potent

102 on, the expression of mutant K-ras in K19(+) gastric epithelial cells can induce chronic inflammation

103 Attachment of the bacterium to polarized gastric epithelial cells causes damage to microvilli and

104 lori up-regulates spermine oxidase (SMOX) in gastric epithelial cells, causing oxidative stress-induc

105 eceptor proteins in solubilized membranes of gastric epithelial cells, class II major histocompatibil

106 When cocultured with gastric epithelial cells, clinical strains of H. pylori

107 by immunohistochemistry and in H. pylori/AGS gastric epithelial cell coculture supernatants by Wester

108 sms of the p27 decrease, using AGS and MKN28 gastric epithelial cells cocultured with H. pylori strai

109 Similar data were also observed in primary gastric epithelial cells confirming the results obtained

110 gastric adenocarcinoma, possibly by altering gastric epithelial cell cycle events and/or gastrin secr

111 ost response interact in the pathogenesis of gastric epithelial cell damage.

112 Laser capture microdissection of human gastric epithelial cells demonstrated expression of SMO(

113 for normal levels of gastric acid secretion, gastric epithelial cell differentiation, and development

114 Shh (Sonic hedgehog) regulates gastric epithelial cell differentiation.

115 s mediating the actions of growth factors on gastric epithelial cell differentiation.

116 Transactivation of gastric epithelial cell EGF receptors may be instrumenta

117 otype when naive T cells were incubated with gastric epithelial cells exposed to H. pylori.

118 e transcriptase-PCR we determined that MKN45 gastric epithelial cells express low but detectable amou

119 T cells, it was important to establish human gastric epithelial cells expressed those surface ligands

120 In 34 specimens, residual normal gastric epithelial cells (foveolar cells) were present f

121 is a gastric tumor suppressor that protects gastric epithelial cells from damage but can promote inv

122 , apoptosis, and DNA damage were measured in gastric epithelial cells from H. pylori-infected Egfr(wa

123 Similarly, B7-2 expression was higher on gastric epithelial cells from H. pylori-infected tissues

124 ore, HpGroES-induced IL-8 release by primary gastric epithelial cells from TLR4(-/-) mice was signifi

125 ntify mechanisms by which Shh might regulate gastric epithelial cell function and differentiation.

126 Helicobacter pylori-induced gastric epithelial cell (GEC) apoptosis is a complex pro

127 own to be highly expressed on the surface of gastric epithelial cells (GEC) during H. pylori infectio

128 Gastric epithelial cells (GEC) play an important role du

129 osis and increases APE-1 expression in human gastric epithelial cells (GEC).

130 ce with a conditional knockout of IKKbeta in gastric epithelial cells (GECs) and myeloid cells, and e

131 Gastric epithelial cells (GECs) are the primary target f

132 arcinogenic mechanisms and is upregulated on gastric epithelial cells (GECs) during H. pylori exposur

133 Gastric epithelial cells (GECs) express the class II maj

134 ter Helicobacter pylori infection in humans, gastric epithelial cells (GECs) undergo apoptosis due to

135 Absence of RUNX3 expression from normal gastric epithelial cells (GECs), the progenitors to GC,

136 tein myeloid cell leukemia 1 (Mcl1) in human gastric epithelial cells (GECs).

137 901), but less cytotoxicity to non-malignant gastric epithelial cells GES1.

138 protein (BMP) signaling in the regulation of gastric epithelial cell growth and differentiation by ge

139 Moreover, during infection of gastric epithelial cells, H. pylori induce intracellular

140 In cultured gastric epithelial cells, H. pylori induced transcriptio

141 When cocultured with AGS gastric epithelial cells, H. pylori strain 60190, which

142 Both cultured gastric epithelial cells (HFE145 and NCI-N87) and primar

143 BMPs are therefore important regulators of gastric epithelial cell homeostasis.

144 cells in the stomach and the maintenance of gastric epithelial cell identity.

145 nvestigated phagocyte clearance of apoptotic gastric epithelial cells in H. pylori infection.

146 facilitates anchorage-independent growth of gastric epithelial cells in soft agar.

147 In vivo, MMP-7 was expressed in gastric epithelial cells in specimens from 80% of cag(+)

148 Gastric epithelial cells in vitro and in vivo are shown

149 selectively increase MMP-7 protein levels in gastric epithelial cells in vitro and in vivo.

150 H. pylori infection activates NF-kappa B in gastric epithelial cells in vitro and in vivo.

151 acute mucosal inflammation, and adherence to gastric epithelial cells in vitro induces expression of

152 H. pylori stimulates expression of MMP-7 in gastric epithelial cells in vitro.

153 xin, VacA, can cause multiple alterations in gastric epithelial cells, including cell death.

154 variety of phenotypic responses in cultured gastric epithelial cells, including the expression of pr

155 e factor CagA; ectopic expression of CagA in gastric epithelial cells increased phosphorylation of HD

156 chanisms leading to upregulation of MMP10 in gastric epithelial cells induced by H. pylori Infection

157 We then used primary human gastric epithelial cells induced to undergo apoptosis by

158 zed by an abundant inflammatory response and gastric epithelial cell injury.

159 Following adhesion of Helicobacter pylori to gastric epithelial cells, intracellular signaling leads

160 c Ca(2+) mobilization within the restituting gastric epithelial cells is a central signal driving sma

161 Increased apoptotic death of gastric epithelial cells is a hallmark of Helicobacter p

162 Adherence of Helicobacter pylori to cultured gastric epithelial cells is associated with several cell

163 astric cancer, and adherence of H. pylori to gastric epithelial cells is critical for induction of in

164 process for which adherence of H. pylori to gastric epithelial cells is critical.

165 -8; however, the mechanism(s), especially in gastric epithelial cells, is not well understood.

166 Interaction of H pylori with gastric epithelial cells leads to robust up-regulation o

167 Gastric epithelial cells liberate prostaglandin E(2) in

168 EGF on PKC, Ras, and ERK activities in a rat gastric epithelial cell line (RGM1).

169 In addition, the CXCR4-negative gastric epithelial cell line AGS became highly responsiv

170 Adherence of Helicobacter pylori to the gastric epithelial cell line AGS strongly induces expres

171 Adherence of Helicobacter pylori to the gastric epithelial cell line AGS strongly upregulated ex

172 transcriptomes of mGEPs and a control mouse gastric epithelial cell line revealed that, upon infecti

173 Treatment of the rat gastric epithelial cell line RGM1 with transforming grow

174 study, we show that in vitro infection of a gastric epithelial cell line with EBV alters growth prop

175 stomach epithelial cells (ImSt) and a human gastric epithelial cell line, AGS cells, as well as wild

176 ut (IFN-gamma(-/-)) mouse model and a murine gastric epithelial cell line, GSM06, we demonstrated tha

177 s markers associated with differentiation of gastric epithelial cell lineages.

178 ssion of B7-1 and B7-2 was detected on human gastric epithelial cell lines and freshly isolated epith

179 its receptors in vivo and with a variety of gastric epithelial cell lines during infection with H. p

180 DNA damage (8-oxoguanosine) were measured in gastric epithelial cell lines infected with cagA(+) or c

181 Human gastric epithelial cell lines or cells isolated from muc

182 mma was expressed and functionally active in gastric epithelial cell lines sensitive to H. pylori-ind

183 The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragm

184 The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori

185 ma, which increases class II MHC expression, gastric epithelial cell lines were exposed to H. pylori

186 tissues, as well as in GC-derived and normal gastric epithelial cell lines.

187 ssion and promoter methylation status in six gastric epithelial cell lines.

188 ing of PE-conjugated urease to class II MHC+ gastric epithelial cell lines.

189 s, and inflammatory responses, activation of gastric epithelial cell MAP kinases by H. pylori cag+ st

190 ue injury, we asked whether MMP secretion by gastric epithelial cells may contribute to gastric injur

191 upregulation of PAI-1 in H. pylori-infected gastric epithelial cells may contribute to the carcinoge

192 We found that interaction of H. pylori with gastric epithelial cells, mediated via the cag pathogeni

193 ithelial cells, AGS cells, and human primary gastric epithelial cells (obtained from patients undergo

194 ith these findings, HO-1 is downregulated in gastric epithelial cells of patients infected with cagA(

195 s infected with cagA(+) H. pylori but not in gastric epithelial cells of patients infected with cagA(

196 region of p65 showed activated NF-kappa B in gastric epithelial cells of patients with H. pylori gast

197 nate TAS2Rs for caffeine, was shown in human gastric epithelial cells of the corpus/fundus and in HGT

198 (gp130) receptor in inflammation-associated gastric epithelial cell oncogenic transformation, which

199 Gastric epithelial cells or colonies were co-cultured wi

200 7.13 or its pgdA(-) isogenic mutant with AGS gastric epithelial cells or HEK293 epithelial cells expr

201 fection would lead to increased apoptosis of gastric epithelial cells, possibly in response to free r

202 position to influence decision-making among gastric epithelial cell precursors and to modulate the m

203 pylori urease B subunit to CD74 expressed on gastric epithelial cells presents a novel insight into a

204 sults may explain heterogeneity in levels of gastric epithelial cell proliferation and apoptosis foun

205 ylori infection disrupts the balance between gastric epithelial cell proliferation and apoptosis, whi

206 Helicobacter pylori cag+ strains enhance gastric epithelial cell proliferation and attenuate apop

207 -catenin, p120, and PPARdelta, which promote gastric epithelial cell proliferation via activation of

208 These studies demonstrate that gastric epithelial cells recognize and respond to H. pyl

209 The mechanisms through which gastric epithelial cells recognize this organism are unc

210 carcinogenesis, how H. pylori reduces p27 in gastric epithelial cells remains unknown.

211 lts indicate that attachment of H. pylori to gastric epithelial cells resembles that of enteropathoge

212 t hBD-2 is a component of the regulated host gastric epithelial cell response to H. pylori infection

213 epithelial damage site that are essential to gastric epithelial cell restitution in vivo.

214 the monitoring of Ca(2+) mobilization during gastric epithelial cell restitution.

215 , and enzyme activity of SMO(PAOh1) in human gastric epithelial cells, resulting in DNA damage and ap

216 cs, cell migration, and proliferation in rat gastric epithelial cell (RGM1) and smooth muscle cell (A

217 Adherence of H. pylori to gastric epithelial cells seems to be required for bacter

218 n understanding the role of CagA in altering gastric epithelial cell signaling pathways.

219 ortant lipo-polysaccharide (LPS) receptor in gastric epithelial cell signaling transduction and plays

220 ori infection has an antiapoptotic effect in gastric epithelial cells that appears to involve Akt sig

221 Recombinant urease induced apoptosis in gastric epithelial cells that express class II MHC molec

222 decrease in p53 levels increased survival of gastric epithelial cells that had sustained DNA damage.

223 A/A increased Ca(2+) permeation in gastric epithelial cells; the increase was blocked by NM

224 H. pylori induces DAF expression in human gastric epithelial cells; therefore, we sought to define

225 ammatory effector heme oxygenase-1 (HO-1) in gastric epithelial cells through a pathway that requires

226 ter pylori CagA protein is translocated into gastric epithelial cells through a type IV secretion sys

227 factor that Helicobacter pylori inject into gastric epithelial cells through a type IV secretion sys

228 IFN-gamma also induced autophagy in gastric epithelial cells through increased expression of

229 HGF triggers activation of the COX-2 gene in gastric epithelial cells through phosphorylation of c-Me

230 bacter pylori causes numerous alterations in gastric epithelial cells through processes that are depe

231 ction, and may enhance the susceptibility of gastric epithelial cells to carcinogenic conversion.

232 ter and ADAM17 activity were measured in AGS gastric epithelial cells transfected with HKalpha promot

233 ylori infection is associated with increased gastric epithelial cell turnover and is a risk factor fo

234 Gastric epithelial cell turnover was no different after

235 pylori infection is associated with altered gastric epithelial cell turnover.

236 reatment led to the reemergence of all major gastric epithelial cell types and restoration of glandul

237 ulation of intracellular pH in each of these gastric epithelial cell types.

238 In vitro studies in gastric epithelial cells using dupA -deleted and -comple

239 Interactions between CagL and host gastric epithelial cell via integrins are required for t

240 H. pylori CagA is translocated into gastric epithelial cells via a type IV secretion pathway

241 A/A affects gastric epithelial cell viability by allowing excessive

242 at the HpGroES-induced IL-8 release by human gastric epithelial cells was dependent on activation of

243 l and H. pylori -infected gastric mucosa and gastric epithelial cells was determined by in situ hybri

244 of this molecule in adhesion of H. pylori to gastric epithelial cells was investigated.

245 The binding of urease to human gastric epithelial cells was reduced by anti-class II MH

246 Gastric epithelial cells were co-cultured with H pylori

247 Gastric epithelial cells were cocultured with Helicobact

248 MKN28 gastric epithelial cells were cocultured with the H pylo

249 AGS gastric epithelial cells were cultured alone or in the p

250 Gastric epithelial cells were cultured to confluence and

251 the role of oxidative stress in cell death, gastric epithelial cells were exposed to various strains

252 AGS gastric epithelial cells were infected with cag(+) toxig

253 Gastric epithelial cells were isolated from the entire s

254 se this receptor as a point of attachment to gastric epithelial cells, which lead to IL-8 production.

255 g cytotoxin (VacA) inhibits proliferation of gastric epithelial cells, which suggests that H pylori m

256 , also caused extensive Ca(2+) permeation of gastric epithelial cells, which was blocked when NMDA-re

257 nt expression and activation of PPARdelta in gastric epithelial cells, which were mediated by the cag

258 Infection of cultured gastric epithelial cells with a wild-type but not an iso

259 Gastric epithelial cells with DNA damage that were negat

260 Coculture of gastric epithelial cells with H. pylori grown under high

261 Experimental coculture of gastric epithelial cells with the strains containing the

262 Co-culture of MKN28 gastric epithelial cells with the wild-type H. pylori ca

263 We co-cultured gastric epithelial cells with wild type H. pylori strain

264 By in vitro infection of gastric epithelial cells with wild-type and VacA-deficie

265 We cocultured gastric epithelial cells with wild-type H. pylori, isoge