Back to Search
Start Over
A smad signaling network regulates islet cell proliferation
- Source :
- Diabetes. January 1, 2014, Vol. 63 Issue 1, p224, 13 p.
- Publication Year :
- 2014
-
Abstract
- Pancreatic β-cell loss and dysfunction are critical components of all types of diabetes. Human and rodent β-cells are able to proliferate, and this proliferation is an important defense against the evolution and progression of diabetes. Transforming growth factor-β (TGF-β) signaling has been shown to affect β-cell development, proliferation, and function, but β-cell proliferation is thought to be the only source of new β-cells in the adult. Recently, β-cell dedifferentiation has been shown to be an important contributory mechanism to β-cell failure. In this study, we tie together these two pathways by showing that a network of intracellular TGF-β regulators, smads 7, 2, and 3, control β-cell proliferation after β-cell loss, and specifically, smad7 is necessary for that β-cell proliferation. Importantly, this smad7-mediated proliferation appears to entail passing through a transient, nonpathologic dedifferentiation of β-cells to a pancreatic polypeptide--fold hormone-positive state. TGF-β receptor II appears to be a receptor important for controlling the status of the smad network in β-cells. These studies should help our understanding of properly regulated β-cell replication. Diabetes 2014;63:224-236 | DOI: 10.2337/db13-0432<br />New pancreatic β-cells form in response to a loss of β-cell mass, and this formation of new β-cells is thought to be an important defense against the evolution and progression [...]
Details
- Language :
- English
- ISSN :
- 00121797
- Volume :
- 63
- Issue :
- 1
- Database :
- Gale General OneFile
- Journal :
- Diabetes
- Publication Type :
- Periodical
- Accession number :
- edsgcl.355150464
- Full Text :
- https://doi.org/10.2337/db13-0432