ライフサイエンスコーパス: islet cell

1 ibraries, each from an individual pancreatic islet cell.

2 structs transduced in MIN6 cells and primary islet cells.

3 ing pancreas development as well as in adult islet cells.

4 m stage cells (CXCR4+ cells), and pancreatic islet cells.

5 ents IGF-1-induced survival of primary mouse islet cells.

6 lored whether Hes3 also regulates pancreatic islet cells.

7 distinct spatial-temporal patterns in rodent islet cells.

8 transcription factor in developing and adult islet cells.

9 and human pancreas and sorted primary human islet cells.

10 r without (n = 8) intraabdominally engrafted islet cells.

11 omers in pancreatic rat insulinoma and human islet cells.

12 ility of (18)F-fallypride as a PET agent for islet cells.

13 entiation into exocrine acinar and endocrine islet cells.

14 ntiate them, i.e., switch their lineage into islet cells.

15 spensable for the function of differentiated islet cells.

16 us as a gene delivery vehicle for pancreatic islet cells.

17 ival of the second wave of hormone-producing islet cells.

18 models for the differentiation of pancreatic islet cells.

19 precursors failed to mature into functional islet cells.

20 ine Neurog3 expression in hormone-expressing islet cells.

21 exit the cell cycle, and differentiate into islet cells.

22 or RNA sequencing of single mouse pancreatic islet cells.

23 without various indirect effects from other islet cells.

24 demonstrate an acinar cell defect but normal islet cells.

25 ted insulin secretion (GSIS) and survival of islet cells.

26 of live-cell phenotypes in single developing islet cells.

27 , cardiomyocytes, and insulin-producing beta islet cells.

28 aimed to assess these findings in East-Asian islet-cells.

29 secretion by increasing oxidative stress in islets cells.

30 tein-coupled receptors that are expressed by islets cells.

31 ferentiated hESCs as compared with CXCR4+ or islets cells.

32 ifferentiation from acinar, centroacinar and islet cells, accompanied by activation of Notch1 signali

33 Experiments were carried out with single islet cells adherent to chimeric proteins made of functi

34 on of menin in pretumor beta-cells increases islet cell adhesion and reduces cell migration.

35 n beta-cell reconstitution from heterologous islet cells after near-total beta-cell loss in mice.

36 T cells secreting IL-4 or IL-10 specific for islet cell Ag, and causes peripheral deletion of beta-ce

37 vide islet cells with glutamate, (b) protect islet cells against high extracellular glutamate concent

38 n insulin-producing beta-cells in a model of islet cell aggregate formation.

39 roughout the rat genome in normal pancreatic islet cells, allowing us to identify the changes that oc

40 ed in cytokine-treated, HLA class II matched islet cells alone.

41 nhbb or addition of activin B stimulates rat islet cell and beta-cell proliferation, and the activin

42 ates Pdx-1-stimulated proliferation of total islet cells and beta cells.

43 the cell cycle during the differentiation of islet cells and demonstrate that the subsequent down-reg

44 uppressed NF-kappaB activation in both human islet cells and immune cells.

45 SAs bound to allogeneic targets expressed by islet cells and induced their destruction in vitro; howe

46 activation of this pathway is detrimental to islet cells and likely promotes damaging autoimmunity an

47 involved in the terminal differentiation of islet cells and maintenance of islet mass.

48 (18)F-fallypride bound to isolated islet cells and pancreatic sections with an endocrine or

49 and contain time-series expressions in human islet cells and rat INS-1E cells.

50 ODY genes in the development of pancreas and islet cells and to evaluate their significance in regula

51 a reciprocal interaction between pancreatic islet cells and vascular endothelial cells (EC) in which

52 ed with an augmented number of proliferative islet cells and with resistance to streptozotocin-induce

53 eart, lung, liver, pancreas, intestinal, and islet cells), and (c) the application of antibody testin

54 ssion of TRB3 84R in mouse beta cells, human islet cells, and the murine beta cell line MIN6 revealed

55 iabetes-associated autoantibodies, including islet cell antibodies (ICAs), reflect adaptive immunity,

56 were analyzed using radiobinding assays and islet cell antibodies with immunofluorescence during a m

57 atter was defined as repeated positivity for islet-cell antibodies plus for at least 1 of 3 other dia

58 Seventy-two islet cell antibody-negative nondiabetic Hispanic women

59 CD8(+) T-cell responses against islet cell antigens, thought to play a central role in d

60 . 9.1%+/-1.1%, P=0.004), and a lower rate of islet cell apoptosis (20.5%+/-2.8% vs. 7.6%+/-2.3%, P=0.

61 GABA reduced human islet cell apoptosis in culture, such that the yield of

62 TCDC did not change islet cell apoptosis.

63 he protective mechanism in berberine against islet cell apoptosis.

64 ttachment and growth of primary human or rat islet cells as monolayers on glass surfaces.

65 Adhesion tests showed that islet cells attached to N-cad/Fc and E-cad/Fc acquired,

66 e 3 years from 22 case children in whom anti-islet cell autoantibodies developed, and 22 matched cont

67 0.5 and 2 years in the children in whom anti-islet cell autoantibodies developed.

68 ssociated antigen-2 antibodies (IA-2As), and islet cell autoantibodies were measured at time of diagn

69 these autoantibodies did not correlate with islet cell autoantibodies.

70 and 22 matched control children who remained islet cell autoantibody-negative in follow-up.

71 No differences between anti-islet cell autoantibody-positive and -negative children

72 ICA69 (islet cell autoantigen 69 kDa) is a protein implicated i

73 Although several islet cell autoantigens are known, the breadth and spect

74 erogeneity in autoantibody responses against islet cell autoantigens including two polymorphic varian

75 f the microbiome in the pathogenesis of anti-islet cell autoimmunity and type 1 diabetes.

76 the gut microbiome in children in whom anti-islet cell autoimmunity developed.

77 Evidence of anti-islet cell autoimmunity in type 1 diabetes appears in th

78 e conclude that hypoglycemia in SCHAD-CHI is islet cell-autonomous.

79 Total pancreatectomy and islet cell autotransplantation (TPIAT) has been increasi

80 y plays a critical role in the regulation of islet cell biology.

81 ival of both MIN6 beta-cells and dissociated islet cells, both at a very low cell-packing density (<

82 anc) mice also had some minor alterations in islet cells, but beta-cell development was not affected.

83 tes (GG) were coencapsulated with pancreatic islet cells by using protamine sulfate as a clinical-gra

84 To investigate whether primary islet cells can produce EXOs, we isolated cells from the

85 , we used the RIP1-Tag2 (RT2) mouse model of islet cell carcinogenesis to identify a genetic locus th

86 differentiation and development, as well as islet cell carcinogenesis.

87 ry neoplasm generated is a highly metastatic islet cell carcinoma of the pancreas.

88 progression, driving the destruction of beta-islet cells, causing hyperglycemia and ultimately death.

89 duced dominant tolerance to porcine neonatal islet cell cluster (NICC) xenografts in mice.

90 perturbed endocrine cell differentiation and islet cell clustering in VEGF-A overexpressing embryos.

91 Neonatal islet cell clusters (ICCs) from INSLEA29Y transgenic (LE

92 While alpha and beta cells formed islet cell clusters in control embryos at E16.5, the inc

93 nd (3) diabetic patients receiving fetal pig islet cell clusters xenograft together with a kidney all

94 To test this hypothesis, we examined islet cell composition in a streptozotocin (STZ)-induced

95 e set of islet preparations, we found a mean islet cell composition of 54.5%+/-1.2% insulin-positive,

96 ometry for assessing beta-cell apoptosis and islet cell composition on serial sections of intact isol

97 eration and insulin secretion of dissociated islet cells, contributing to the reduced beta-cell mass

98 n important regulator of gene expression and islet cell coordination.

99 cell type exhibits hallmarks of its primary islet cell counterpart including cell-specific expressio

100 ADK-Is is cell type-selective: treatment of islet cell cultures with ADK-Is increases replication of

101 erleukin-1beta- and interferon-gamma-induced islet cell death in vitro.

102 Diabetes, but the link of hIAPP structure to islet cell death remains elusive.

103 Flow-sorted ALDH(+) islet cells demonstrate impaired glucose-induced insulin

104 differentiation and islet development while islet cell-derived angiogenic factors promote EC recruit

105 nifested as a pancreatic insulitis with beta-islet cell destruction and systemic glucose intolerance.

106 Nrp2 mutant islet cells developed in proper numbers, but had defects

107 r signals identified factors that stimulated islet cell development.

108 Islet cells differentiate properly in Galphao(-/-) mutan

109 lls (EC) in which EC-derived signals promote islet cell differentiation and islet development while i

110 in-1 (Ang1), or angiopoietin-2 (Ang2) during islet cell differentiation and islet development.

111 w that the transcription factor Rfx6 directs islet cell differentiation downstream of Neurog3.

112 ndodermal progenitor cells towards endocrine islet cell differentiation during embryogenesis.

113 necessary and sufficient to induce endocrine islet cell differentiation from embryonic pancreatic pro

114 transcription factors that are essential for islet cell differentiation have been well characterized;

115 scription factor neurogenin3 (Ngn3) triggers islet cell differentiation in the developing pancreas.

116 Galphao is not required for endocrine islet cell differentiation, but it regulates the number

117 Neurog3 target genes that are essential for islet cell differentiation, maturation, and function.

118 o parse out the spatiotemporal regulation of islet cell differentiation, we used a Neurog3-Cre allele

119 Thus, mammalian pancreatic islet cells display cell-type-specific epigenomic plasti

120 Diannexin was administered to islet cell donors shortly before pancreas harvest, added

121 ofound dose-dependent deleterious effects on islet cell engraftment.

122 ion in sites that might be more favorable to islet cell engraftment.

123 We found that islet cells expressed the genes encoding all of the prod

124 Here we show that islet cells expressing insulin, glucagon, or somatostati

125 stinct from others in regard to temporal and islet cell expression pattern, with beta-cells affected

126 of pancreatic progenitor cells to adopt the islet cell fate.

127 tory program to correctly specify pancreatic islet cell fates.

128 ucose-regulated hormone secretion, and human islet cells follow a similar pattern.

129 promote growth, function, and engraftment of islet cells following transplantation.

130 eptozotocin (STZ)-treated primary pancreatic islet cells from ICR mice to unravel the protective mech

131 psulation system to protect the transplanted islet cells from immune system attack while allowing the

132 cretion resulting from changes in pancreatic islet cell function and/or mass.

133 study indicated that, from the standpoint of islet cell function, linagliptin would be more effective

134 ors associated with pancreas development and islet cell function, we analyzed how an endogenous delet

135 s toxicity on both renal and pancreatic beta-islet cell function.

136 omoters and enhancers to repress alternative islet cell genes including ghrelin, glucagon, and somato

137 nd in silico replications of mouse and human islet cell genes were performed.

138 type 1 diabetic recipients of an intraportal islet-cell graft under maintenance immunosuppression (IS

139 ressants in 35 type 1 diabetic recipients of islet cell grafts prepared from a median of 6 donors (ra

140 Allosensitization to cultured human islet cell grafts was low when assessed by CDC assay but

141 2 diabetes and contributes to the failure of islet cell grafts.

142 The formation of hIAPP amyloid plaques near islet cells has been linked to the death of insulin-secr

143 sis and proliferation, but during adulthood, islet cells have a very slow turnover.

144 We found a decrease in pancreatic islet cell hyperplasia, fat accumulation in the liver, a

145 as and four additional positive lesions (two islet-cell hyperplasia and two uncharacterised lesions)

146 One true negative (islet-cell hyperplasia) and one false negative (malignan

147 omotes glucose-stimulated insulin secretion, islet cell hypertrophy, and islet cell proliferation, th

148 he genetic and molecular factors controlling islet cell identity and function.

149 oliferating betaTC-6 cells, but not in human islet cells; (ii) down-regulation of ZBED6 in betaTC-6 c

150 ls at embryonic stages or in Pdx1-expressing islet cells in adults impairs endocrine function, a phen

151 id bilayers, but appear to have no effect on islet cells in culture.

152 ptide-lipid interactions with its effects on islet cells in culture.

153 s) ILT3 induce allogeneic tolerance to human islet cells in humanized NOD/SCID mice.

154 B-dependent fashion) and translated by human islet cells in response to in vitro inflammatory stimuli

155 ed destruction of the insulin-producing beta-islet cells in the pancreas.

156 IL15/IL-15Ralpha expression was increased in islet cells in the prediabetic stage, and inhibition of

157 eptor (D(2)/D(3)R)-based PET method to study islet cells in the rat pancreas and in islet cell transp

158 direct role in the death of pancreatic beta-islet cells in type II diabetes.

159 s surrogate beta-cells and human HLA-A*24(+) islet cells in vitro.

160 e long-term insulin secretion by xenografted islet cells in vivo, and represent a novel contrast agen

161 t on the NOD background despite an increased islet cell infiltrate with markedly increased numbers of

162 A landscape with multiple intra-islet cell interconversion events is emerging, offering

163 rable leakage of the contrast agent into the islet cell interstitium.

164 et amyloid polypeptide (hIAPP) in pancreatic islet cells is implicated in the pathogenesis of type II

165 et, that insulin secretion, intrinsic to the islet cells, is a key mechanism underlying the associati

166 g pancreas and is later restricted to mature islet cells, is involved in the terminal differentiation

167 ssion of miR-29a/b/c in MIN6 and dissociated islet cells led to impairment in glucose-induced insulin

168 Snord116 may play a role in islet cell lineage specification.

169 The genetic determinants of acinar and islet cell lineages are somewhat well defined; however,

170 TC1 (alphaTC1) and Beta-TC-6 (betaTC6) mouse islet cell lines are cellular models of islet (dys)funct

171 E-seq data from islets to that from five non-islet cell lines revealed approximately 3,300 physically

172 ucose and lipid impair beta cell function in islet cell lines, cultured rodent and human islets, and

173 A noninvasive method that measures islet cell loss and also tracks the fate of transplanted

174 entify how acinar cell proteases cause human islet cell loss before and after transplantation of impu

175 Islet cell loss in the pancreas results in diabetes.

176 ent with DXM improved islet insulin content, islet cell mass and blood glucose control.

177 of A1AT to impure islet cultures maintained islet cell mass, restored insulin levels, and preserved

178 m a more rigid structure, often encasing the islet cell mass.

179 cell differentiation, but also for promoting islet cell maturation and maintaining islet function.

180 ted the hypothesis that enriching pancreatic islet cell membranes with EPA, thereby reducing arachido

181 d that a multiparametric approach focused on islet cell metabolic state, mitochondrial integrity, and

182 roach using objective assessments focused on islet cell mitochondrial integrity and in vitro function

183 When mimicked in newborn islet cells, modifications in the level of specific micr

184 The islet cell monolayer cultures on glass stably maintain d

185 initial bursting discharge, Ih currents, and islet cell morphology.

186 tion of glucagon secretion where neighboring islet cells negatively regulate glucagon secretion throu

187 ssion of miR-26a in mice increases postnatal islet cell number in vivo and endocrine/acinar colonies

188 tes to the alteration of beta-cell identity, islet cell numbers and morphology, and gene expression b

189 this pathogenic process was active in human islet cells obtained from donors with type 2 diabetes; t

190 ) is a highly amyloidogenic protein found in islet cells of patients with type II diabetes.

191 ly transcript 1epsilon (RAE1epsilon) in beta-islet cells of the pancreas, we found that RAE1 expressi

192 nolayers of adherent and well-spread primary islet cells on glass coverslips is required for detailed

193 Expression of hIAPP in purified monkey islet cells or a murine beta cell line resulted in pro-h

194 ely 40-microm) pseudoislets using all of the islet cells or only some of the cell types, which allowe

195 e treated with alloxan to destroy pancreatic islet cells, or mock-treated with vehicle, and maintaine

196 We found that islet cell organization, beta-cell mass, and beta-cell f

197 They suggested a secretin-like hormone of islet cell origin explains WDS and achlorhydria.

198 ), 67 SNPs for type 2 diabetes in pancreatic islet cells (P = 0.003) and the liver (P = 0.003), and 1

199 direct effects of autonomic nervous input on islet cell physiology cannot be studied in the pancreas.

200 down-regulation of Neurog3 allows the mature islet cell population to expand.

201 d expression of HLA class II on transplanted islet cells potentially causing antidonor sensitization

202 ted the hypothesis that HLA-A24 molecules on islet cells present preproinsulin (PPI) peptide epitopes

203 Human islet cells process and present PPI(3-11), rendering the

204 ells expressed Sema3a, while central nascent islet cells produced the semaphorin receptor neuropilin

205 Organ growth and pancreatic islet cell proliferation and mass were examined in sheep

206 slets, Inhbb overexpression stimulates total islet cell proliferation and potentiates Pdx-1-stimulate

207 Accordingly, a higher frequency of islet cell proliferation was detected in Ad5-infected is

208 eported that Pdx-1 overexpression stimulates islet cell proliferation, but the mechanism remains uncl

209 sulin secretion, islet cell hypertrophy, and islet cell proliferation, the latter exclusively through

210 s sufficient to stimulate both rat and human islet cell proliferation.

211 Pancreatic islet cells provide the major source of counteractive en

212 Assays for assessing human islet cell quality, which provide results before transpl

213 ve broader implications on the regulation of islet cell ratios and their ability to effectively respo

214 When cultured, murine islet cells reassociate to form pseudoislets, which reco

215 enes, including those involved in regulating islet cell recovery and proliferation, and identify addi

216 th coincident enhancement of nuclear Nrf2 in islet cells, reduced beta-cell oxidative stress, and pre

217 ian model can be used to define pathways for islet-cell regeneration in humans.

218 Islet cell replacement can effectively treat diabetes bu

219 f disease would require strategies combining islet cell replacement with immunotherapy that are curre

220 ent strategy to examine age-associated human islet cell replication competence and reveal mechanisms

221 Furthermore, a GABAA-R PAM promoted human islet cell replication in vitro.

222 of the embryonic endocrine pancreas and the islet cell replication that occurs in an adult animal.

223 ls of exogenous GABA further increased human islet cell replication.

224 The national Islet Cell Resource Center Consortium provides human pan

225 arkably, miR-375 normalization in LP-derived islet cells restores beta-cell proliferation and insulin

226 Dispersed islet cells secrete aberrant levels of glucagon and insu

227 Acute islet cell secretory responses were determined under fas

228 origins in different germ layers, pancreatic islet cells share many common developmental features wit

229 Guided by an observation that dispersed islet cells spread and adhere well on glass surfaces in

230 ing' genes tested were expressed in purified islet-cell subpopulations with a notable variability, de

231 Applying the method to mouse pancreatic islet-cell subsets, we detected both expected and unknow

232 human gene expression and epigenomic data in islet cell subtypes constitutes a truly valuable resourc

233 ld pancreas preservation and their impact on islet cell survival and function.

234 GABA improved human islet cell survival and had suppressive effects on human

235 elin promotes pancreatic beta-cell and human islet cell survival and prevents diabetes in streptozoto

236 fluorescence-enhanced (NIR-FE) detection of islet cell-targeting autoantibodies.

237 tecture between alphaTC1/betaTC6 and primary islet cells that can be leveraged in functional (epi)gen

238 lity to sophisticated analyses of pancreatic islet cells that reveal new biological insights, as demo

239 by the disruption of cellular homeostasis in islet cells through the formation of membrane-active oli

240 ial signaling axis that instructs developing islet cells to disperse throughout the pancreas.

241 islets, mouse islets, and dissociated mouse islet cells to restore euglycemia, 3) the generation of

242 ed pseudoislets reconstituted from dispersed islet cells to study alpha-cells with and without variou

243 resentation of insulin epitopes by dispersed islet cells to T cells was impaired, and (iii) the devel

244 h repeated positivity for antibodies against islet cells) together with positivity for at least one o

245 tment option for type 1 diabetes, pancreatic islet cell transformation has been hindered by immune sy

246 ification could potentially lead to improved islet cell transplant outcomes.

247 The use of tacrolimus in our islet-cell transplant protocol caused an initial 20% red

248 The promise of islet cell transplantation cannot be fully realized in t

249 Islet cell transplantation has limited effectiveness bec

250 analysis plans for future pivotal trials of islet cell transplantation in type 1 diabetes.

251 nts with type 1 diabetes of longer duration, islet cell transplantation may be more effective than me

252 vs placebo (RR 0.60; 95% CI 0.41-0.86), and islet cell transplantation vs medical therapy (RR 0.25;

253 ed inflammatory loss of graft function after islet cell transplantation.

254 red a risk factor for liver, intestinal, and islet cell transplantation.

255 e loss of functional islets after allogeneic islet cell transplantation.

256 ed its efficacy in a rhesus macaque model of islet cell transplantation.

257 study islet cells in the rat pancreas and in islet cell transplantation.

258 ing of allograft injury in humans undergoing islet cell transplantation.

259 CXCR4-CXL12 axis, to promote engraftment of islet cell transplantation.

260 -2 diabetes, and also reduces the success of islet cell transplantation.

261 oon retrograde transvenous obliteration, and islet cell transplantation.

262 so show that for encapsulated rat pancreatic islet cells transplanted into streptozotocin-treated dia

263 2 diabetes and contributes to the failure of islet cell transplants, however the mechanisms of IAPP-i

264 amyloid formation in type 2 diabetes and in islet cell transplants.

265 ng somatic gene transfer in a mouse model of islet cell tumorigenesis, we demonstrate that RHAMM isof

266 neuroendocrine tumors (pNET), also known as islet cell tumors, exhibit a wide range of biologic beha

267 I on blood vessels of spontaneous pancreatic islet-cell tumors in RIP-Tag2 transgenic mice.

268 is essential for pancreatic development and islet cell type differentiation.

269 othesis is based on the assumption that each islet cell type has a specific pattern of miRNA expressi

270 n transcription factor that is essential for islet cell type specification and mature beta cell funct

271 standing of the molecular components of each islet cell type that govern islet (dys)function, particu

272 A fifth islet cell type, the ghrelin-producing epsilon cells, is

273 on factor Neurogenin3 (Ngn3) is required for islet-cell type specification.

274 ng Rfx6 failed to generate any of the normal islet cell types except for pancreatic-polypeptide-produ

275 differentiation of the beta-cells and other islet cell types from pancreatic endoderm, but the genet

276 e intra-islet interactions between different islet cell types functions not only to reduce the superf

277 of this homologue reduced the numbers of all islet cell types including the insulin-producing beta-ce

278 icantly affecting the proportions of various islet cell types that do form.

279 c basis for the observed plastic identity of islet cell types, and have implications for beta-cell re

280 ene in mice leads to loss of most pancreatic islet cell types, the functional consequences of Pax6 lo

281 n were detected in macrophages but not other islet cell types.

282 ical to ensure there is a correct balance of islet cell types.

283 ights into genes and pathways characterizing islet cell types.

284 odeficiency mice received transplanted human islet cells under the kidney capsule and adoptively tran

285 Diminishment of functional islet cells' VTCN1 is caused by the active proteolysis b

286 whether cadherin-mediated adhesion of human islet cells was affected by insulin secretagogues and ex

287 Expression of GABA(A)R subunits in islet cells was confirmed by immunohistochemistry.

288 Expression of GABA(A)Rs in islet cells was investigated by quantitative PCR, immuno

289 We observed that cadherin expression in islet cells was not affected by insulin secretagogues.

290 human leukocyte antigen (HLA) class I on the islet cells, we examined its expression in subjects with

291 as initiates their differentiation to mature islet cells, we examined the role of Neurog3 in cell cyc

292 The viability and glucose responsiveness of islet cells were assessed in vitro, and in vivo insulin

293 Cadaveric human islet cells were encapsulated with alginate, poly-l-lysi

294 validate the approach, single rat pancreatic islet cells were rapidly analyzed with optically guided

295 Rat islet cells were transplanted into the spleen and visual

296 448 islet-cells were captured from three East-Asian non-diab

297 Slc1a2) has been hypothesized to (a) provide islet cells with glutamate, (b) protect islet cells agai

298 ed 622 cells, allowing identification of 341 islet cells with high-quality gene expression profiles.

299 in cytokine-treated and virus-infected human islet cells, with up-regulation of gene networks involve

300 reduces the overall production of endocrine islet cells without significantly affecting the proporti