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Expression data comparing adult human islets to human embryonic stem cell-derived insulin-positive and insulin-negative cells

ABSTRACT: The study was completed to compare expression profiles of primary human beta cells (in the form of adult human islets), to the expression profile of hESC-derived beta-like cells. A HES3 line modified by homologous recombination to express GFP under the insulin promoter allowed us to FACS sort the hESC-derived cells into purified insulin-positive (presumably beta-like cells), and insulin-negative populations.

ORGANISM(S): Homo sapiens

PROVIDER: GSE40709 | GEO | 2012/09/09

SECONDARY ACCESSION(S): PRJNA174727

REPOSITORIES: GEO

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Expression data comparing adult human islets to human embryonic stem cell-derived insulin-positive and insulin-negative cells

Project description:The study was completed to compare expression profiles of primary human beta cells (in the form of adult human islets), to the expression profile of hESC-derived beta-like cells. A HES3 line modified by homologous recombination to express GFP under the insulin promoter allowed us to FACS sort the hESC-derived cells into purified insulin-positive (presumably beta-like cells), and insulin-negative populations. Expression profile of adult human islets from cadaveric donors is compared to insulin-positive and insulin-negative populations of hESC-derived beta-like cells

2012-09-09 | E-GEOD-40709 | biostudies-arrayexpress

Gene expression data from Min6 cells grown in serum containing and serum free condtions following Hes3 knock down

Project description:The basic helix-loop-helix (bHLH) transcription factor hairy and enhancer of split (Hes3) is a member of the Hes/Hey gene family that regulates developmental processes in progenitor cells from various tissues. We demonstrated the Hes3 expression in mouse pancreatic tissue, suggesting it may have a role in modulating beta-cell function. We employed a transfection approach to address specific functions of Hes3. Hes3 RNA interference opposed the growth of the mouse insulinoma cell line Min6. Western blotting and PCR approaches specifically showed that Hes3 RNA interference opposes the expression of Pdx1 and insulin. Likewise, Hes3 knock down reduced evoked insulin release from Min6 cells.

2014-12-23 | GSE64449 | GEO

Gene expression data from Min6 cells grown in serum containing and serum free condtions following Hes3 knock down

2014-12-23 | E-GEOD-64449 | biostudies-arrayexpress

Expression data from Min6 cells maintained under different culture conditons that affect Hes3 expression and localization

Project description:The basic helix-loop-helix (bHLH) transcription factor hairy and enhancer of split (Hes3) is a member of the Hes/Hey gene family that regulates developmental processes in progenitor cells from various tissues. We demonstrated the Hes3 expression in mouse pancreatic tissue, suggesting it may have a role in modulating beta-cell function. We employed the mouse insulinoma cell line MIN6 to perform gene expression profiles in conditions known to modulate Hes3 based upon our previous work using neural stem cell cultures. In these conditions, cells showed elevated Hes3 expression and nuclear localization, grew efficiently and showed higher evoked insulin release responses, compared to serum-containing conditions. They also exhibited higher expression of the transcription factor Pdx1 and insulin.

2014-12-23 | GSE64444 | GEO

Hypothalamic oxidative stress provokes leptin and insulin resistance [Islets]

Project description:The relationship between loss of hypothalamic function and onset of diabetes mellitus remains elusive. Therefore, we generated a targeted oxidative-stress murine model utilizing conditional knockout of selenocysteine-tRNA (Trsp) using rat insulin promoter-driven-Cre (RIP-Cre). These Trsp-knockout (TrspRIPKO) mice exhibit deletion of Trsp in both hypothalamic cells and pancreatic β-cells leading to increased hypothalamic oxidative stress and severe insulin resistance. Leptin signals were suppressed and numbers of proopiomelanocortin-positive neurons in the hypothalamus were decreased. In contrast, a Trsp-knockout mouse (TrspIns1KO) expressing Cre specifically in pancreatic β-cells, but not in the hypothalamus, did not display insulin and leptin resistance, demonstrating a critical role of the hypothalamus in the onset of diabetes mellitus. Nrf2 (NF-E2-related-factor-2) regulates antioxidant gene expression. Gene-driven increase in Nrf2 signaling suppressed hypothalamic oxidative stress and improved insulin and leptin resistance in TrspRIPKO mice. Thus, Nrf2 harbors the potential to prevent the onset of diabetic mellitus by reducing hypothalamic oxidative damage.

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Expression data from Min6 cells maintained under different culture conditons that affect Hes3 expression and localization

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2014-12-23 | E-GEOD-64444 | biostudies-arrayexpress

Beta cell markers of aging have heterogeneous distribution in islets and are induced by insulin resistance

Project description:Our hypothesis was that at any given point in time, islets will contain differing populations of beta cells at different stages of their lifecycle, with further changes occurring with metabolic stress and aging. We examined subpopulations of beta cells isolated from MIP-GFP mice on the basis of their insulin transcriptional activity and in their expression of p16Ink4a. In addition, using aging C57Bl/6 mice as a model, markers of beta cell aging were identified and validated: Igf1r and Cd99 expression increased with age, whereas Kcnq5 was decreased with age. These markers were correlated with an age-related decline in function. The functional aging of beta cells was accelerated by S961, an antagonist to the insulin receptor, which induced insulin resistance. Particularly surprising was the finding of marked islet heterogeneity as demonstrated with the marked staining differences of the markers: Igf1r, Cd99 and Kcnq5. These novel findings about beta cell and islet heterogeneity, and how they change with age, open up an entirely new set of questions that must be addressed about the pathogenesis of type 2 diabetes. The present study has identified new markers of aging in beta cells and found that the expression of these and other markers can be increased by insulin resistance. This provides insight into how insulin resistance might accelerate the death of beta cells. In addition, striking heterogeneity among islets was found, which opens up new ways to think about islet biology and the pathogenesis of T2D.

2017-03-22 | GSE72753 | GEO

Reduced basal insulin secretion from islets isolated from tafazzin deficient mice is associated with reduced mitochondrial function

Project description:Tafazzin is a transacylase which causes the content and molecular structure of cardiolipin (CL) to be altered in the inner mitochondrial membrane. The enzymatic machinery responsible for oxidative respiration are localized to the inner mitochondrial membrane and require CL for activity. As a result, tafazzin is critical for maintaining mitochondrial function. In beta-cells, which are the insulin secreting cells in pancreatic islets, mitochondrial function is linked to insulin secretion. We previously established that tafazzin knock-down mice were lean and maintained insulin sensitivity compared to the obese insulin resistant control litter mates. However, it was unknown whether tafazzin deficiency also influenced insulin secretion in the establishment of the lean phenotype. Using X week-old mice, we ascertained that the number of beta-cells was similar between genotypes. Ex vivo insulin secretion under low glucose conditions was reduced (52%) from islets isolated from tafazzin knock-down mice. Consistent with this tafazzin knock-down mice exhibited reduced fasting insulin plasma insulin levels. Measurement of mitochondrial oxygen consumption revealed that basal oxygen consumption was reduced (58%) in islets from tafazzin-deficient animals. The addition of etomoxir, an inhibitor of mitochondrial fatty acid translocation, significantly elevated basal mitochondrial respiration (5-fold) in islets from tafazzin knockdown mice, indicating a significant fatty acid-mediated inhibitory effect. In contrast, etomoxir lacked any measurable effect on control wild-type islets. The altered mitochondrial function identified in taffazin knock-down islets was not associated with reduced CL content or elevated oxyCL species. Our experiments indicate that tafazzin plays a key role in regulating normal islet beta-cell function.

2021-07-31 | GSE136242 | GEO

Transcriptional profiling by array of INSULIN-expressing cells derived from INS-GFP human embryonic stem cells under different differentiation and culture conditions

Project description:Differentiation of INSGFP/w hESCs using published protocols demonstrated that all GFP+ cells co-expressed insulin, confirming the fidelity of the reporter gene. INS-GFP+ cells also co-expressed glucagon and somatostatin, confirming prior studies regarding the polyhormonal nature of early hESC derived insulin-expressing cells. INSGFP/w hESCs were employed to develop a 96 well format spin Embryoid Body (EB) differentiation protocol that utilized the recombinant protein based fully defined medium, APEL. Like INS-GFP+ cells generated with other methods, those derived using the spin EB protocol expressed a collection of pancreatic related transcription factors including ISL1, PAX6 and NKX2.2. However, in contrast to previous methods, the spin EB protocol yielded INS-GFP+ cells that also co-expressed the beta-cell transcription factor, NKX6.1 and comprised a substantial proportion of monohormonal insulin+ cells.

2012-02-02 | E-MEXP-3378 | biostudies-arrayexpress