Journal
DIABETES
Volume 62, Issue 3, Pages 887-895Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db12-0451
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Funding
- National Institutes of Health [P01DK-49210]
- Commonwealth of Pennsylvania (Center for Excellence in Regenerative Medicine) [4100043362]
- National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases / Beckman Research Center Integrated Islet Distribution Program [10028044]
- American Diabetes Association (ADA-Takeda Mentor-Based Postdoctoral Fellowship)
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Elucidating the mechanism underlying the poor proliferative capacity of adult pancreatic beta-cells is critical to regenerative therapeutic approaches for diabetes. Here, we show that the microRNA (miR)-7/7ab family member miR-7a is enriched in mouse adult pancreatic islets compared with miR-7b. Remarkably, miR-7a targets five components of the mTOR signaling pathway. Further, inhibition of miR-7a activates mTOR signaling and promotes adult beta-cell replication in mouse primary islets, which can be reversed by the treatment with a well-known mTOR inhibitor, rapamycin. These data suggest that miR-7 acts as a brake on adult beta-cell proliferation. Most importantly, this miR-7-mTOR proliferation axis is conserved in primary human beta-cells, implicating miR-7 as a therapeutic target for diabetes. Diabetes. 62:887-895, 2013
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