MicroRNA for treating cancer and asthma

A microRNA that regulates inflammation shows promise as a treatment for inflammatory diseases such as asthma and cancer. The microRNA, known as miR-223, is highly expressed in blood cells that cause inflammation (neutrophils). When they're working correctly, those blood cells protect the body against infections, but sometimes they damage host tissue instead of microbes, causing chronic inflammation and disease.

To uncover the link between miR-223 and inflammation, a Purdue University research team created a zebrafish totally deficient of miR-223. Then they cut off a small chunk of its fin. "The inflammation was really robust," said Qing Deng, a professor of biological sciences at Purdue and corresponding author of the paper. "Neutrophils accumulated at the wound and they just kept coming. This is consistent with the literature, but we wanted to understand why."

Extensive gene expression analysis led them to pathway NF-kB, a protein complex found in nearly all animal cell types that regulates inflammation and cell proliferation. Heightened activation of this pathway is the cause of increased inflammation, although it's limited to the deeper, or basal, layer of the epithelium. This means any therapeutics would need to reach the basal layer to work.

The same pathway plays an important role in human bronchial epithelial cells, which are critical in the development of asthma, according to the study. MiR-223 suppresses the pathway, which means supplementing it to epithelial cells could help control inflammatory disease.
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Pancreatic islets and diabetes treatment

Researchers have discovered new insights into the molecular mechanisms of cell proliferation in juvenile human pancreatic islets, the discovery could lead to new treatments for diabetes. In type 1 and type 2 diabetes, the insulin-producing beta cells found in cell clusters in the pancreas, known as pancreatic islets, are either destroyed or become dysfunctional, leading to insulin deficiency.

Insulin is the hormone responsible for the regulation of blood glucose levels.
Researchers took viable samples of human pancreatic islet cells obtained from both juveniles, defined as age 10 or younger, and from adults, between the age of 20 to 60 years old. The islet cells were transferred into a mouse model lacking an immune system, which allowed the human cells to survive and function for several months.

These types of human islet cells had increased rates of proliferation after transfer into the mouse model, indicating this was an intrinsic property of the juvenile islet cells and not the pancreatic environment. Beta cell growth rate declines with age. Using a drug analogue of glucagon-like peptide 1 (GLP-1), a common clinical treatment for type 2 diabetes, it was shown over a period of four weeks that beta cell proliferation was stimulated only in the juvenile islet cells, but not in the adult cells.

In comparing the islet cells, it was discovered that the GLP-1 receptors were similar in both juvenile and adult pancreatic islets, suggesting that pathways inside the human juvenile islet cells were responsible for the different response in adult islet cells.
Researchers examined the series of interactions among the molecules of a cell that lead to a specific product or change in a cell. They discovered difference in the calcineurin pathway between the juvenile islet cells and the adult islets.
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Diabetes and heart disease are related

Type 2 diabetes is a risk factor for coronary heart disease, CHD Researchers examined the
genome sequence information of some people and discovered 16 new diabetes genetic risk factors, and one new CHD genetic risk factor; showing that the two diseases are related.

They discovered that sites on the genome associated with higher diabetes risk are also associated with higher CHD risk. For eight of these sites, the researchers were able to identify a specific gene variant that influences risk for both diseases.

The shared genetic risk factors affect biological pathways including immunity, cell proliferation, and heart development. Identifying these gene variants linked to both type 2 diabetes and CHD risk in principle opens up opportunities to reduce the risk of both diseases.

The genetic link between the diseases appears to work in one direction, so that risk genes for type 2 diabetes are much more likely to be associated with higher CHD risk than the other way around. Additionally, there could be some pathways where pharmacological lowering of one disease increases the risk of the other.

The researchers also found that diabetes-linked gene variants tend to differ in their apparent effects on CHD risk, depending on their mechanisms. Variants that increase the chance of obesity or high blood pressure, for example, appear to boost CHD risk more strongly than variants that alter insulin or glucose levels.

They discovered that the genomic regions implicated as dual diabetes-CHD risk loci encompass targets of some existing drugs. One such drug is icosapent, an omega-3 fatty acid component of some fish oils, which lowers cholesterol and is sold in concentrated form as a prescription pharmaceutical.
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