ライフサイエンスコーパス: islet

1 contained a higher number of beta-cells per islet.

2 tiates diabetogenicity within the autoimmune islet.

3 released from alpha-cells of the pancreatic islet.

4 are modulated by glucose in mouse pancreatic islets.

5 lucose-stimulated insulin release from donor islets.

6 a protective barrier surrounding pancreatic islets.

7 mulated insulin secretion in mouse and human islets.

8 of active enhancers in both murine and human islets.

9 iled to reach the endocrine cells of grafted islets.

10 s IBMIR and cytokine-induced inflammation in islets.

11 3K27 at loci downregulated in Hnf1alpha-null islets.

12 in mouse and human beta-cell lines and human islets.

13 n that overlaps a stretch-enhancer active in islets.

14 ps a predicted enhancer region in pancreatic islets.

15 nsure the survival and function of engrafted islets.

16 lls and increases insulin secretion from T2D islets.

17 we constructed computational models of human islets.

18 at enables the transplantation of pancreatic islets.

19 n source of proinflammatory cytokines within islets.

20 beta-cell function and maturity in isolated islets.

21 are impacted during aging in mouse and human islets.

22 inhibited insulin secretion only from mouse islets.

23 minate, migrate radially and cluster to form islets.

24 ARC affects JNK signaling in amyloid-forming islets.

25 ux by altering the chemotactic milieu in the islets.

26 Here, we show that, although endogenous islet ACE2 expression is sparse, its inhibition abrogate

27 We applied these procedures to analysis of islet Ag-reactive CD4(+) memory T cells from the blood o

28 Treatment with islet Ag-specific regulatory T cells led to a marked dec

29 Mutant Nrp2 islets aggregated centrally and failed to disperse radia

30 C) B cell numbers in naive mice and hastened islet allograft rejection.

31 ocked, led to HSC mobilization and prolonged islet allograft survival.

32 islet (NPI) xenografts compared with rhesus islet allografts at 1 hour, 24 hours, and 7 days.

33 transplant tolerance induction to mismatched islet allografts.

34 s over the potential of the BM as a site for islet allotransplantation.

35 S was used to identify individual pancreatic islet alpha and beta cells, which were then targeted for

36 ted in Hnf1alpha-null islets and Nkx2.2-null islets, among others.

37 Because islet amyloid increases c-Jun N-terminal kinase (JNK) pa

38 Islet amyloid is present in more than 90% of individuals

39 (Abeta) and tau in the brain during AD, and islet amyloid polypeptide (IAPP) in pancreatic islets in

40 Islet amyloid polypeptide (IAPP) is responsible for cell

41 Aggregation of islet amyloid polypeptide (IAPP), a peptide hormone co-s

42 umulate misfolded aggregates composed of the islet amyloid polypeptide (IAPP), its role in the diseas

43 of the intrinsically disordered polypeptide islet amyloid polypeptide (IAPP), which is associated wi

44 od glucose levels, higher insulin, and lower islet amyloid polypeptide accumulation were observed.

45 mbly of amyloid-beta, alpha synuclein, human islet amyloid polypeptide and prions, the peptides and p

46 iously characterized alpha-helical cytotoxic islet amyloid polypeptide oligomers which interact with

47 rmediate during the aggregation of the human islet amyloid protein (hIAPP or amylin), the protein ass

48 We show that NUCB1 inhibits aggregation of islet-amyloid polypeptide associated with type 2 diabete

49 In the clinical settings of islet and renal transplantation, donor exosomes with res

50 olled in the TEDDY study who were tested for islet and tissue transglutaminase autoantibodies, respec

51 ecretion both in human and murine pancreatic islets and in clonal beta cells in a dose- and time-depe

52 eatic islets is a harsh microenvironment for islets and it lacks the ability to retrieve the graft.

53 es and genes downregulated in Hnf1alpha-null islets and Nkx2.2-null islets, among others.

54 nocytic origin of CD11c(+) cells in inflamed islets and suggest that therapeutic regulatory T cells d

55 Ccl8 were persistently elevated in inflamed islets and the influx of CD11c(+) cells was partially de

56 cholesterol accumulation in human pancreatic islets and the INS-1 insulinoma cell line.

57 zed regions of metabolic activity across the islet, and these affect the way in which beta-cells elec

58 Expression of KCNB1 appears reduced in T2D islets, and further knockdown of KCNB1 does not inhibit

59 y expressed SOX family protein in pancreatic islets, and mutations in Sox4 are associated with an inc

60 ing are poorly understood in mouse and human islets, and the impact of aging on intraislet communicat

61 tially methylated regions (DMRs) in diabetic islets, and to investigate the function of DMRs in islet

62 In neprilysin-deficient mouse islets, angiotensin-(1-7) and neprilysin-derived degrada

63 As the islet approaches its mature state, heterogeneity diminis

64 Whereas islet architecture in rodents is distinctly different fr

65 ts the large loss of islets that occurs when islets are infused into the portal vein.

66 While adult islets are thought to contain functionally mature beta c

67 tio [HR], 0.98; 95% CI, 0.95-1.01), multiple islet autoantibodies (HR, 0.99; 95% CI, 0.95-1.03), or t

68 eived as a T cell-driven autoimmune disease, islet autoantibodies are the best currently available bi

69 Islet autoimmunity and CD autoimmunity were defined as b

70 widely applied to total pancreatectomy with islet autotransplantation (TPIAT).

71 The islet basement membrane (BM) influences islet function a

72 g shows that the beta-cells in the embryonic islet become functional during early zebrafish developme

73 somes with respective tissue specificity for islet beta cells and renal epithelial cells were reliabl

74 sing stage led to immature and dysfunctional islet beta cells carrying abnormal chromatin marking in

75 the formation of all pancreatic cell types, islet beta-cell development, and adult islet beta-cell f

76 Islet beta-cell dysfunction and aggressive macrophage ac

77 ypes, islet beta-cell development, and adult islet beta-cell function.

78 e novel findings to Pdx1 gene regulation and islet beta-cell maturation postnatally.

79 ys and was recently found to be expressed in islet beta-cells.

80 er, our comprehensive analysis of pancreatic islet bioenergetics reveals that Drp1 does not control i

81 resource for comprehensive understanding of islet biology and diabetes pathogenesis.

82 , and to investigate the function of DMRs in islet biology.

83 may be for the exploration of revascularized islet biology.

84 ompromised as a consequence of an incomplete islet BM, which has implications for islet survival and

85 ing-regulatory RNA-binding proteins in human islets, brain, and other human tissues, and we identifie

86 tem in obesity; inflammation within diabetic islets, brain, liver, gut, and muscle; the role of infla

87 cked exendin-4-stimulated insulin release in islets but also lowered insulin levels while increasing

88 L3 GALR3) were abundantly expressed in mouse islets but present only at low levels in human islets, s

89 f of principle of in vivo targeting of human islets by [(11)C]AZ12204657 was shown in the immunodefic

90 A positive correlation between islet cadmium content and both age (p = 0.048, R(2) = 0.

91 aft outcomes, but only conformal coated (CC) islets can be implanted in these sites in curative doses

92 In isolated islets, carbachol and PACAP/VIP synergistically promote

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

94 tory program to correctly specify pancreatic islet cell fates.

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

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

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

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

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

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

101 The islet cell monolayer cultures on glass stably maintain d

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

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

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

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

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

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

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

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

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

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

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

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

114 without various indirect effects from other islet cells.

115 inflammation, pancreatic islet morphometry, islet cellular composition, and inflammation.

116 ed to decreased Atf5 transcript, and primary islet ChIP-sequencing localized PDX1 to the Atf5 promote

117 ZDF islets contain elevated levels of CB1R, interleukin-1bet

118 y elevated beta-cell [Ca(2+)]i in Abcc8(-/-) islets contributes to the alteration of beta-cell identi

119 ied miR-708 as the most upregulated miRNA in islets cultured at low glucose concentrations, a setting

120 In vitro, islets cultured under 140 mm Hg oxygen showed reduced ce

121 Islets deficient in GATA6 activity display decreased ins

122 se results open the potential for using s.c. islet delivery as a treatment option for type I diabetes

123 HFD-islets demonstrated evidence of oxidative stress and DNA

124 Finally, HFD-islets demonstrated reduced expression of multiple ribos

125 eater islet injury with further reduction in islet density, decreased relative beta-cell number, and

126 al cell-type-specific features of pancreatic islet (dys)function and provides a critical resource for

127 environmental, and cellular contributions to islet (dys)function and T2DM pathogenesis.

128 mponents of each islet cell type that govern islet (dys)function, particularly the less abundant delt

129 Genes linked to rare and common forms of islet dysfunction and diabetes were expressed in the del

130 let-like extracellular matrix (Matrigel; MG) islet encapsulation (PEG MG) to improve capsule immunois

131 Islet encapsulation may allow transplantation without im

132 We find that islet endocrine cells from older donors display increase

133 ferentiate or become reprogrammed into other islet endocrine cells.

134 nd, therefore, have the potential to improve islet engraftment and survival.

135 n studies (GWASs) and recent developments in islet (epi)genome and transcriptome profiling (particula

136 higher yield (5535 +/- 830 and 2582 +/- 925 islet equivalent/g, P < .05) and less undigested tissue

137 immunodeficient mice at a marginal dose (500 islet equivalents).

138 ction led to a marked decrease in transplant islet exosome signal along with distinct changes in exos

139 RIP-LCMV islets express CXCL10 after isolation and maintain CXCL1

140 coding, and pseudogenes) was associated with islet expression levels.

141 In human type 1 diabetes pancreatic islets, fasting conditions reduce PKA and mTOR activity

142 At later stages, younger beta-cells join the islet following differentiation from post-embryonic prog

143 The transplantation of pancreatic islets, following the Edmonton Protocol, is a promising

144 We exposed isolated rat islets for 1 h to increasing glucose concentrations and

145 In addition, islets from Ab+ donors were larger and contained a highe

146 we developed a strategy to macroencapsulate islets from different sources that allow their survival

147 pared these findings with gene expression in islets from donors with normal glucose tolerance and hyp

148 dence of decreased IL-6 pathway signaling in islets from donors with type 2 diabetes.

149 Thus, we isolated islets from either normal or CXCL10-deficient RIP-LCMV m

150 Islets from human donors and from mice were studied usin

151 We identified 25,820 DMRs in islets from individuals with T2D.

152 hanism for rescuing the oscillations seen in islets from mice deficient in K(ATP) channels.

153 creatic beta-cell dysfunctions, we evaluated islet function and glucose metabolism regulation in DKO

154 The islet basement membrane (BM) influences islet function and survival and is a critical marker of

155 Islet function and survival may be compromised as a cons

156 This is the first report indicating that islet function can be improved by using low-dose rC1rC2

157 These results show that human islet function declines with aging, which can reduce ins

158 immediate posttransplant period and impaired islet function in the longer term.

159 These DMRs cover loci with known islet function, e.g., PDX1, TCF7L2, and ADCY5 Importantl

160 6 mice did not affect multiple parameters of islet function, including glucose response, insulin cont

161 ications for therapeutics aimed at improving islet function.

162 m reduced proliferative capacity and reduced islet function.

163 immunogenicity while allowing physiological islet function.

164 gestion and poor islet recovery but improved islet function.

165 ators in orchestrating insulin secretion and islet gene transcription has been demonstrated recently.

166 for the therapeutic potential of PSC-derived islets generated by blastocyst complementation in a xeno

167 ermore, in vivo deletion of miR-204 promoted islet GLP1R expression and enhanced responsiveness to GL

168 Our comprehensive human and mouse islet GPCR atlas has demonstrated that species differenc

169 strated that species differences do exist in islet GPCR expression and function, which are likely to

170 Taken together, AAT significantly improves islet graft survival after intraportal islet transplanta

171 ive transfer of the same DSAs did not affect islet graft survival in murine models.

172 ence the cellular composition locally in the islet graft, thereby playing a role in the autoimmune de

173 with vascular sequestration of DSAs protects islet grafts from humoral rejection.

174 flammation and loss of beta-cell function in islet grafts.

175 Islet homogenates immunodepleted with anti-IAPP-specific

176 f beta-cells and ectopic expression of other islet hormones, including somatostatin and glucagon.

177 proghrelin in association with reductions in islet, hypothalamic, and stomach PC1 content.

178 tion without immunosuppression, but thus far islets in large microcapsules transplanted in the perito

179 lso observed dose-specific effects of BPA on islets in males.

180 We suggest that human islets in T2D display changes reminiscent of dedifferent

181 let amyloid polypeptide (IAPP) in pancreatic islets in T2D.

182 use biosensor to assess the quality of donor islets in terms of their insulin production efficiency,

183 nd roles of macrophage polarity shift within islets in the context of T2D pathology and beta cell hea

184 capsules improved engraftment of allogeneic islets in the IP site, but resulted deleterious in the E

185 scaffold maintains viability and function of islets in the subcutaneous site.

186 nhibits insulin secretion in mouse and human islets in vitro and in vivo in rodents.

187 ctive oxygen species in both mouse and human islets in vitro.

188 etermined in isolated fetal ovine pancreatic islets in vitro.

189 in several endocrine cells of the pancreatic islet, including glucagon secreting alpha-cells, but par

190 In mouse islets, incubation with ML351 improved glucose-stimulate

191 lls was because of a significant decrease in islet infiltration of mononuclear cells.

192 , impairment of beta-cell function and mass, islet inflammation (i.e., insulitis), and autoantibodies

193 -specific expression of IP-10 contributed to islet inflammation and loss of beta-cell function in isl

194 e cellular and molecular mechanisms by which islet inflammation develops and causes beta cell dysfunc

195 than db/db mice, despite displaying similar islet inflammation.

196 ductal marker CK19 vs. control subjects, and islet inflammatory cell infiltrates, independently of th

197 CFRD pancreata exhibited greater islet injury with further reduction in islet density, de

198 In conclusion, in islets, intact angiotensin-(1-7) is not the primary medi

199 ion and survival and is a critical marker of islet integrity following rodent islet isolation.

200 as transplantation site for human pancreatic islets is a harsh microenvironment for islets and it lac

201 ecent reports that the insulin production of islets is mechanosensitive, these findings open up an ex

202 in the survival and function of transplanted islets is unknown.

203 s within the cellular infiltrates around the islet isografts.

204 l marker of islet integrity following rodent islet isolation.

205 ined the CC composition and explored PEG and islet-like extracellular matrix (Matrigel; MG) islet enc

206 Immunoprecipitation of ARC from mouse islet lysates showed ARC binds JNK, suggesting interacti

207 The number of intra-islet macrophages is increased in T2D, and these cells a

208 n beta-cells of channelrhodopsin2-expressing islets, mapped the [Ca(2+)]i response, and correlated th

209 mTORC2 (with adaptor protein Rictor) impacts islet mass and architecture.

210 The change in islet mass in different stages of type 2 diabetes (T2D)

211 t with expected stratification of pancreatic islet mass were examined in relation to individuals with

212 a surrogate imaging biomarker of pancreatic islet mass.

213 rical indenter and found that insulitis made islets mechanically soft compared with controls.

214 g, demonstrated by insulin released from the islet microtissues in response to a glucose load applied

215 teatosis, metabolic inflammation, pancreatic islet morphometry, islet cellular composition, and infla

216 The marginal dose of 400 islets (n = 5) induced normoglycemia in 20%.

217 Transplantation of 800 (n = 5) and 1200 islets (n = 5) into the scaffold reversed diabetes in re

218 efficacious because all 800 (n = 5) and 1200 islets (n = 5) recipients and 40% of the 400 islets (n =

219 islets (n = 5) recipients and 40% of the 400 islets (n = 5) recipients became normoglycemic within 8

220 e early immune responses to neonatal porcine islet (NPI) xenografts compared with rhesus islet allogr

221 Misregulated hormone secretion from the islet of Langerhans is central to the pathophysiology of

222 TRM cells were also sporadically found in islets of control subjects.

223 tested whether EVs isolated from pancreatic islets of healthy patients and patients with T2D modulat

224 Thus, the macrophages of the islets of Langerhans are poised to mount an immune respo

225 l profiles of macrophages that reside in the islets of Langerhans of 3-wk-old non-obese diabetic (NOD

226 on of the resident macrophages of pancreatic islets of Langerhans that lasted for several weeks.

227 persed in multiple micro-organs known as the islets of Langerhans.

228 sponse and insulin secretion dynamics of the islets of Langerhans.

229 onsible for cell depletion in the pancreatic islets of Langherans, and for multiple pathological cons

230 etes development, it was not clear how human islets of T2D patients would respond to linagliptin trea

231 iation between early-life antibiotic use and islet or celiac disease (CD) autoimmunity in genetically

232 insulin replacement therapies (such as human islet or stem cell-derived beta cell transplantation) wi

233 oimmunity were defined as being positive for islet or tissue transglutaminase autoantibodies at 2 con

234 These results suggest that a risk of islet or tissue transglutaminase autoimmunity need not i

235 ing of insulin secretion from isolated mouse islets or INS-1 beta-cells.

236 after activation with pooled immunodominant islet peptides.

237 hat a high number of genes with key roles in islet physiology, including regulators of glucose sensin

238 Pancreatic islets produce and secrete cytokines and chemokines in r

239 human endothelial cells and neonatal porcine islets prolonged time to clot formation.

240 resulted in pancreas underdigestion and poor islet recovery but improved islet function.

241 We observed that islets release multiple inflammatory mediators in patien

242 We found that rat and human pancreatic islets release the intracellular beta-cell autoantigens

243 em insufficient for isolating the numbers of islets required to treat diabetes in a rat model.

244 e dominant alpha2delta subunit in pancreatic islets, results in glucose intolerance and diabetes with

245 Additionally, low-dose RCEM islets retained better morphology (confirmed with scanni

246 , our data suggest that SK1 is important for islet revascularization following transplantation and re

247 enome and transcriptome variation across 112 islet samples to produce dense cis-expression quantitati

248 38 cells from nondiabetic (ND) and T2D human islet samples.

249 ot reflect loss of GLP-1R signaling in adult islets, since Ex-4 treatment stimulated insulin secretio

250 ater glucose induced-insulin release, larger islet size and beta-cell mass, and more proliferative an

251 Islet size and insulin content in pancreata of A2AAR-def

252 lets but present only at low levels in human islets, so that it reads (GALR3) and galanin inhibited i

253 that uses quartz glass nanopillars to anchor islets, solving a long-standing problem of keeping tissu

254 ransgenic mouse studies confirmed that donor islet-specific expression of IP-10 contributed to islet

255 sites previously identified by ChIP-seq for islet-specific transcription factors, enhancer regions,

256 The islet-specific zinc transporter ZnT8 mediates zinc enric

257 To measure islet stiffness, we used atomic force microscopy (AFM) a

258 Six hundred syngeneic islets subcutaneously transplanted into the prevasculari

259 The transplanted islets successfully normalized and maintained host blood

260 production in both non-diabetic and diabetic islets, suggesting a positive role of linagliptin in mod

261 he potential treatments for T1DM but limited islet survival and their impaired function pose limitati

262 omplete islet BM, which has implications for islet survival and transplanted graft longevity.

263 splantation site under the skin and supports islet survival.

264 e have more pancreatic beta cells and larger islets than db/db mice, despite displaying similar islet

265 ulin independence reflects the large loss of islets that occurs when islets are infused into the port

266 ion of genomic CpG sites in human pancreatic islets, the tissue of primary pathogenic importance for

267 -density ischemia were investigated in human islets to develop a detailed profile of early ischemia i

268 ostatin secretion and respiration from human islets, to be enhanced during palmitate treatment at nor

269 NA methylation landscape in human pancreatic islets, to identify differentially methylated regions (D

270 leased, and high levels correlated with poor islet transplant outcomes.

271 roves islet graft survival after intraportal islet transplantation by mitigation of coagulation in IB

272 e report that the efficiency of subcutaneous islet transplantation in a Lewis rat model is significan

273 We showed that islet transplantation in confined well-vascularized site

274 Pancreatic islet transplantation is a promising clinical treatment

275 etes as well as during islet transplantation.Islet transplantation is considered one of the potential

276 In intraportal islet transplantation models using mouse and human islet

277 s a suitable polymer to create an artificial islet transplantation site under the skin and supports i

278 ous subcutaneous insulin infusion (CSII) and islet transplantation to reduce hypoglycemia and glycemi

279 development of more effective strategies for islet transplantation without immunosuppression.

280 lity, negatively affecting outcomes of human islet transplantation.

281 l state of type-1 diabetes as well as during islet transplantation.Islet transplantation is considere

282 nflammatory mediators in patients undergoing islet transplants within hours of infusion.

283 on-essential divalent metal content of human islets under normal environmental exposure conditions ha

284 immunodeficient mice transplanted with human islets under the kidney capsule.

285 s, as well as in human and murine pancreatic islets, via AKT/BCL2 signaling.

286 Islet viability after acute ischemic exposure was reduce

287 ell activity and glucagon secretion in human islets, we constructed computational models of human isl

288 transplantation models using mouse and human islets, we demonstrated that alpha-1 antitrypsin (AAT; P

289 Human islets were exposed in a pairwise model simulating high-

290 Rat islets were transplanted in the PDLLCL scaffold in a dia

291 Human islets were transplanted under the KC of diabetic immuno

292 lex mediating the maturation and function of islets, whereas mTORC2 (with adaptor protein Rictor) imp

293 occurs in the connective tissue outside the islet, which remains more or less intact.

294 ation site on graft outcomes of encapsulated islets will aid in the development of more effective str

295 on fringing reefs around two Pacific remote islets with large seabird colonies.

296 n of zinc and other divalent metals in human islets with rs13266634 genotype and demographic characte

297 ough in vitro viability and functionality of islets within MicroMix and Double capsules were comparab

298 n associated with brain death (BD) decreases islet yield and quality, negatively affecting outcomes o

299 T2DM risk allele C is associated with higher islet zinc levels and support prior evidence of cadmium'

300 C/C at rs13266634 is associated with higher islet Zn concentration (C/C genotype: 16792 +/- 1607, n