AsianScientist (Jan. 31, 2017) – A study by Tokohu University researchers has identified two new types of microRNA (miRNA) that stimulated the proliferation of insulin-producing pancreatic beta (β) cells in mice. This finding, published in EBioMedicine, could one day lead to the development of new diabetes treatment strategies.
First discovered in the 1990s, miRNAs are small, non-coding RNA molecules that help control cellular processes such as differentiation, proliferation and death. As such, they are potential targets for new treatments for diseases including hepatitis C, cancer and possibly diabetes.
Diabetes is caused when pancreatic β-cells, which produce the hormone insulin to regulate blood sugar levels, are destroyed by the immune system (type 1 diabetes), or are unable to produce sufficient insulin for adequate glucose control (type 2 diabetes).
Bone marrow (BM) transplantation has been shown to promote β-cell proliferation via BM cell to β-cell intercellular communication. However, the molecular mechanisms underlying β-cell regeneration after transplantation are unknown.
Now, Tohoku University researchers have identified two new microRNAs contributing to BM transplantation-induced β-cell regeneration. Using mice that received a BM transplant, the researchers identified 42 miRNAs that were increased in serum exosomes, lipid vesicles which transport miRNAs.
Two of these miRNAs, miR-106b-5p and miR-222-3p, were shown to be secreted by BM cells and their levels were increased in the pancreatic islet cells that produce insulin. Treatment with anti-miRNAs specific for these miRNAs inhibited BM transplantation-induced β-cell regeneration, confirming their role in this process.
When molecules mimicking miR-106b-5p and miR-222-3p were given to mice with insulin-deficient diabetes, it promoted β-cell proliferation, thereby reducing symptoms of diabetes. The researchers concluded that these two miRNAs could be beneficial in regenerative therapies for diabetes.
The article can be found at: Tsukita et al. (2016) MicroRNAs 106b and 222 Improve Hyperglycemia in a Mouse Model of Insulin-Deficient Diabetes via Pancreatic β-Cell Proliferation.
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Source: Tohoku University; Photo: Shutterstock.
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