Cited by 334Pancreatic function and diabetesDiabetes and associated disordersNeurogenesis and neuroplasticity mechanisms

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Cyclins D2 and D1 Are Essential for Postnatal Pancreatic β-Cell Growth

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Kushner, Jake A., Ciemerych, Maria A., Sicinska, Ewa, Wartschow, Lynn M., Teta, Monica, Long, Simon Y., Sicinski, Piotr, White, Morris F.·2005·Molecular and Cellular Biology

DOI 10.1128/mcb.25.9.3752-3762.2005PMC PMC1084308

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Abstract

Regulation of adult beta-cell mass in pancreatic islets is essential to preserve sufficient insulin secretion in order to appropriately regulate glucose homeostasis. In many tissues mitogens influence development by stimulating D-type cyclins (D1, D2, or D3) and activating cyclin-dependent kinases (CDK4 or CDK6), which results in progression through the G(1) phase of the cell cycle. Here we show that cyclins D2 and D1 are essential for normal postnatal islet growth. In adult murine islets basal cyclin D2 mRNA expression was easily detected, while cyclin D1 was expressed at lower levels and cyclin D3 was nearly undetectable. Prenatal islet development occurred normally in cyclin D2(-/-) or cyclin D1(+/-) D2(-/-) mice. However, beta-cell proliferation, adult mass, and glucose tolerance were decreased in adult cyclin D2(-/-) mice, causing glucose intolerance that progressed to diabetes by 12 months of age. Although cyclin D1(+/-) mice never developed diabetes, life-threatening diabetes developed in 3-month-old cyclin D1(-/+) D2(-/-) mice as beta-cell mass decreased after birth. Thus, cyclins D2 and D1 were essential for beta-cell expansion in adult mice. Strategies to tightly regulate D-type cyclin activity in beta cells could prevent or cure diabetes.

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Authors: Kushner, J. A., Ciemerych, M. A., Sicinska, E., Wartschow, L. M., Teta, M., Long, S. Y., Sicinski, P., & White, M. F.
Affiliations: Children's Hospital of Philadelphia (US)
Harvard University (US)
Department of Cancer Biology, Dana-Farber Cancer Institute and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115
Howard Hughes Medical Institute (US)
Corresponding author: Kushner, Jake A.
ORCID: Kushner, Jake A.
Ciemerych, Maria A.
White, Morris F.
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 2005-05-01
Volume: 25
Issue: 9
Pages: 3752-3762
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.25.9.3752-3762.2005
PMC: PMC1084308
OpenAlex: W1969459168
Cited by: 334
References: 32
Citations by year: 2026: 2 · 2025: 9 · 2024: 7 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 7 · 2019: 13 · 2018: 9 · 2017: 18 · 2016: 16 · 2015: 17 · 2014: 16 · 2013: 21 · 2012: 21
FWCI: 28.22
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
PubMed Central (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed (publishedVersion)
Funders: Howard Hughes Medical Institute
Charles H. Hood Foundation
Kosciuszko Foundation
Pediatric Endocrine Society
National Institutes of Health (5k11dk002024-02, DK38712)
National Cancer Institute (R01CA083688)
National Institute of Diabetes and Digestive and Kidney Diseases (DK55326, DK 43808, R01DK055326, DK 38712, DK 02024, R01DK038712, DK 064101, K08DK064101, R01DK043808)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: cyclin D2, cyclin D1, cyclin D3, pancreatic beta-cell proliferation, beta-cell mass, impaired glucose tolerance, diabetes mellitus, CDK4, CDK6, G1 cell cycle, pancreatic islets
MeSH terms: Animals, Blood Glucose, Diabetes Mellitus, Glucagon, Insulin, Islets of Langerhans, Male, Gene Expression, Cyclins, Glucose Intolerance, Mice, Knockout, Cyclin D1, Cell Proliferation, Mice, Cyclin D2

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Cyclins D2 and D1 Are Essential for Postnatal Pancreatic β-Cell Growth

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