MicroRNA-7a regulates pancreatic β cell function
Open accessAbstract
Dysfunctional microRNA (miRNA) networks contribute to inappropriate responses following pathological stress and are the underlying cause of several disease conditions. In pancreatic β cells, miRNAs have been largely unstudied and little is known about how specific miRNAs regulate glucose-stimulated insulin secretion (GSIS) or impact the adaptation of β cell function to metabolic stress. In this study, we determined that miR-7 is a negative regulator of GSIS in β cells. Using Mir7a2 deficient mice, we revealed that miR-7a2 regulates β cell function by directly regulating genes that control late stages of insulin granule fusion with the plasma membrane and ternary SNARE complex activity. Transgenic mice overexpressing miR-7a in β cells developed diabetes due to impaired insulin secretion and β cell dedifferentiation. Interestingly, perturbation of miR-7a expression in β cells did not affect proliferation and apoptosis, indicating that miR-7 is dispensable for the maintenance of endocrine β cell mass. Furthermore, we found that miR-7a levels are decreased in obese/diabetic mouse models and human islets from obese and moderately diabetic individuals with compensated β cell function. Our results reveal an interconnecting miR-7 genomic circuit that regulates insulin granule exocytosis in pancreatic β cells and support a role for miR-7 in the adaptation of pancreatic β cell function in obesity and type 2 diabetes.
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GIIS is enhanced in mir-7a knockout mice, despite no obvious effect on [Ca2+]i or the number of docked granules.
“GIIS is enhanced in mir-7a knockout mice (371), despite there being no obvious effect on [Ca2+]i or the number of docked granules.”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [371]
The Results report increased glucose-stimulated insulin secretion in islets from Mir7a2 knockout mice. The Discussion says the enhanced exocytosis could not be explained by changes in intracellular calcium or docked granule number, but those measurements were made in miR-7a-inhibited β cells, not directly in the knockout mice. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMiR-7 is the 2nd most abundant miR in human β-cells.
“MiR-7 is the 2nd most abundant miR in human β-cells.”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [371]
The Results report high miR-7 expression in human pancreatic islets, but do not rank it against other miRNAs in human β-cells. The statement that miR-7a2 is the most abundant member of the miR-7 family concerns variants within that family, not miR-7’s rank among all miRNAs. The claimed second-place ranking is therefore unsupported. (LLM, conf=0.85)
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- Authors
- Latreille, M., Hausser, J., Stützer, I., Zhang, Q., Hastoy, B., Gargani, S., Kerr-Conte, J., Pattou, F., Zavolan, M., Esguerra, J. L. S., Eliasson, L., Rülicke, T., Rorsman, P., & Stoffel, M.
- Affiliations
- Inserm (FR)
- University of Basel (CH)
- Churchill Hospital (GB)
- Université de Lille (FR)
- University of Veterinary Medicine Vienna (AT)
- Corresponding author
- Stoffel, Markus
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2014-05-01
- Volume
- 124
- Issue
- 6
- Pages
- 2722-2735
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC4038573
- OpenAlex
- W2129743050
- Cited by
- 281
- References
- 63
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 17 · 2023: 20 · 2022: 26 · 2021: 27 · 2020: 26 · 2019: 30 · 2018: 32 · 2017: 24 · 2016: 15 · 2015: 35 · 2014: 11
- FWCI
- 28.11
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion, other-oa)
- Funders
- National Science Foundation
- Fondation de l'Avenir pour la Recherche Médicale Appliquée
- Wellcome Trust (095531/Z/11/Z, 095531)
- European Genomic Institute for Diabetes (ANR-10-LABX-46)
- European Foundation for the Study of Diabetes
- Agence Nationale de la Recherche (ANR‐10‐LABX‐46, 10-LABX-46, ANR-10)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (127307)
- Eidgenössische Technische Hochschule Zürich
- Crafoordska Stiftelsen
- Knut och Alice Wallenbergs Stiftelse
- Vetenskapsrådet
- Veterinärmedizinische Universität Wien
- Region Skåne
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- microRNA, pancreatic beta cells, glucose-stimulated insulin secretion, insulin granule exocytosis, SNARE complex, beta-cell dedifferentiation, type 2 diabetes, obesity, islets, beta-cell function
- MeSH terms
- Insulin Secretion, Animals, Diabetes Mellitus, Exocytosis, Humans, Insulin, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Obesity, Mice, Knockout, MicroRNAs, Insulin-Secreting Cells, SNARE Proteins, Mice, Cell Dedifferentiation
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