The DOI matches its OpenAlex record; 28 of the 28 references it cites were found in a registry or an index.
β cell replication is the primary mechanism for maintaining postnatal β cell mass
Open accessAbstract
The endocrine pancreas undergoes major remodeling during neonatal development when replication of differentiated beta cells is the major mechanism by which beta cell mass is regulated. The molecular mechanisms that govern the replication of terminally differentiated beta cells are unclear. We show that during neonatal development, cyclin D2 expression in the endocrine pancreas coincides with the replication of endocrine cells and a massive increase in islet mass. Using cyclin D2-/- mice, we demonstrate that cyclin D2 is required for the replication of endocrine cells but is expendable for exocrine and ductal cell replication. As a result, 14-day-old cyclin D2-/- mice display dramatically smaller islets and a 4-fold reduction in beta cell mass in comparison to their WT littermates. Consistent with these morphological findings, the cyclin D2-/- mice are glucose intolerant. These results suggest that cyclin D2 plays a key role in regulating the transition of beta cells from quiescence to replication and may provide a target for the development of therapeutic strategies to induce expansion and/or regeneration of beta cells.
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Cites
Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction
Chomczynski, P., & Sacchi, N. (1987) · Analytical Biochemistry · doi:10.1016/0003-2697(87)90021-2 · Cited by 46,426
β-Cell Deficit and Increased β-Cell Apoptosis in Humans With Type 2 Diabetes
Butler, A. E., Janson, J., Bonner-Weir, S., Ritzel, R., Rizza, R. A., & Butler, P. C. (2003) · Diabetes · doi:10.2337/diabetes.52.1.102 · Cited by 4,011
Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation
Dor, Y., Brown, J., Martinez, O. I., & Melton, D. A. (2004) · Nature · doi:10.1038/nature02520 · Cited by 2,219
Gu, G., Dubauskaite, J., & Melton, D. A. (2002) · Development · doi:10.1242/dev.129.10.2447 · Cited by 1,518
D-type cyclin-dependent kinase activity in mammalian cells.
Matsushime, H., Quelle, D. E., Shurtleff, S. A., Shibuya, M., Sherr, C. J., & Kato, J. Y. (1994) · Molecular and Cellular Biology · doi:10.1128/mcb.14.3.2066 · Cited by 1,064
Matsushime, H., Ewen, M. E., Strom, D. K., Kato, J.-Y., Hanks, S. K., Roussel, M. F., & Sherr, C. J. (1992) · Cell · doi:10.1016/0092-8674(92)90360-o · Cited by 897
Rane, S. G., Dubus, P., Mettus, R. V., Galbreath, E. J., Boden, G., Reddy, E. P., & Barbacid, M. (1999) · Nature Genetics · doi:10.1038/8751 · Cited by 700 · cited 1×
“The CDK4-null mice also display a defect in β cell proliferation, indicating that CDK4 acts as the requisite partner for cyclin D2 in controlling cell cycle progression in β cells (21).”
BackgroundCyclin D2 is an FSH-responsive gene involved in gonadal cell proliferation and oncogenesis
Sicinski, P., Donaher, J. L., Geng, Y., Parker, S. B., Gardner, H., Park, M. Y., Robker, R. L., Richards, J. S., McGinnis, L. K., Biggers, J. D., et al. (1996) · Nature · doi:10.1038/384470a0 · Cited by 697
Dynamics of β-cell Mass in the Growing Rat Pancreas: Estimation With a Simple Mathematical Model
Finegood, D. T., Scaglia, L., & Bonner-Weir, S. (1995) · Diabetes · doi:10.2337/diab.44.3.249 · Cited by 603
Pancreatic organogenesis — developmental mechanisms and implications for therapy
Edlund, H. (2002) · Nature Reviews Genetics · doi:10.1038/nrg841 · Cited by 523
Cited by
The PI3K/AKT Pathway in Obesity and Type 2 Diabetes
Huang, X., Liu, G., Guo, J., & Su, Z. (2018) · International Journal of Biological Sciences · doi:10.7150/ijbs.27173 · Cited by 1,673
“Activation of the PI3K/AKT pathway promotes insulin secretion form pancreatic β cells [142, 143].”
BackgroundBeta Cell Dysfunction and Insulin Resistance
Cerf, M. E. (2013) · Frontiers in Endocrinology · doi:10.3389/fendo.2013.00037 · Cited by 964
Meier, J. J., Butler, A. E., Saisho, Y., Monchamp, T., Galasso, R., Bhushan, A., Rizza, R. A., & Butler, P. C. (2008) · Diabetes · doi:10.2337/db07-1369 · Cited by 683
Self-citationRecovery from diabetes in mice by β cell regeneration
Nir, T., Melton, D. A., & Dor, Y. (2007) · Journal of Clinical Investigation · doi:10.1172/jci32959 · Cited by 595
Growth and Regeneration of Adult β Cells Does Not Involve Specialized Progenitors
Teta, M., Rankin, M. M., Long, S. Y., Stein, G. M., & Kushner, J. A. (2007) · Developmental Cell · doi:10.1016/j.devcel.2007.04.011 · Cited by 551
Metadata
- Authors
- Georgia, S. K., & Bhushan, A.
- Venue
- Journal of Clinical Investigation
- Publisher
- American Society for Clinical Investigation
- Published
- 2004-10-01
- Volume
- 114
- Issue
- 7
- Pages
- 963-968
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2111404063
- Cited by
- 506
- References
- 28
- FWCI
- 28.47
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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