ArticlePloS one2013
Microarray analysis of novel candidate genes responsible for glucose-stimulated insulin secretion in mouse pancreatic β cell line MIN6.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
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- A Novel Peptide COXCurrent protein & peptide science · 2024Article
- A large-scale functional analysis of genes expressed differentially in insulin secreting MIN6 sublines with high versus mildly reduced glucose-responsiveness.Scientific reports · 2023Article
- Application of In Vitro Models for Studying the Mechanisms Underlying the Obesogenic Action of Endocrine-Disrupting Chemicals (EDCs) as Food Contaminants-A Review.International journal of molecular sciences · 2023Review
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- Importance of Heparan Sulfate Proteoglycans in Pancreatic Islets and β-Cells.International journal of molecular sciences · 2022Review
- MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1.Diabetology & metabolic syndrome · 2022Article
- Using recombinase-mediated cassette exchange to engineer MIN6 insulin-secreting cells based on a newly identified safe harbor locus.Journal of diabetes investigation · 2021Article
- Importance of Both Imprinted Genes and Functional Heterogeneity in Pancreatic Beta Cells: Is There a Link?International journal of molecular sciences · 2021Review
- Establishment of a long-term stable β-cell line and its application to analyze the effect of Gcg expression on insulin secretion.Scientific reports · 2021Article
- Imprinted Genes Impact Upon Beta Cell Function in the Current (and Potentially Next) Generation.Frontiers in endocrinology · 2021Review
- ZIGIR, a Granule-Specific ZnCell reports · 2020Article
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- Exogenous Cytokine-Free Differentiation of Human Pluripotent Stem Cells into Classical Brown Adipocytes.Cells · 2019Article
- Androgen receptor-deficient islet β-cells exhibit alteration in genetic markers of insulin secretion and inflammation. A transcriptome analysis in the male mouse.Journal of diabetes and its complications · 2017Article
- Histone deacetylase regulates insulin signaling via two pathways in pancreatic β cells.PloS one · 2017Article
- Functional Analysis of Novel Candidate Regulators of Insulin Secretion in the MIN6 Mouse Pancreatic β Cell Line.PloS one · 2016Article
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- Hypomethylation of the promoter of the catalytic subunit of protein phosphatase 2A in response to hyperglycemia.Physiological reports · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elucidating the regulation of glucose-stimulated insulin secretion (GSIS) in pancreatic islet β cells is important for understanding and treating diabetes. MIN6 cells, a transformed β-cell line derived from a mouse insulinoma, retain GSIS and are a popular in vitro model for insulin secretion. However, in long-term culture, MIN6 cells' GSIS capacity is lost. We previously isolated a subclone, MIN6 clone 4, from the parental MIN6 cells, that shows well-regulated insulin secretion in response to glucose, glybenclamide, and KCl, even after prolonged culture. To investigate the molecular mechanisms responsible for preserving GSIS in this subclone, we compared four groups of MIN6 cells: Pr-LP (parental MIN6, low passage number), Pr-HP (parental MIN6, high passage number), C4-LP (MIN6 clone 4, low passage number), and C4-HP (MIN6 clone 4, high passage number). Based on their capacity for GSIS, we designated the Pr-LP, C4-LP, and C4-HP cells as "responder cells." In a DNA microarray analysis, we identified a group of genes with high expression in responder cells ("responder genes"), but extremely low expression in the Pr-HP cells. Another group of genes ("non-responder genes") was expressed at high levels in the Pr-HP cells, but at extremely low levels in the responder cells. Some of the responder genes were involved in secretory machinery or glucose metabolism, including Chrebp, Scgn, and Syt7. Among the non-responder genes were Car2, Maf, and Gcg, which are not normally expressed in islet β cells. Interestingly, we found a disproportionate number of known imprinted genes among the responder genes. Our findings suggest that the global expression profiling of GSIS-competent and GSIS-incompetent MIN6 cells will help delineate the gene regulatory networks for insulin secretion.
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