Researchers from the University of Michigan and the University at Buffalo have discovered a gene that appears to be responsible for causing arthritis and the inflammation that results.
The study, published online April 16 in Science Translational Medicine, was conducted by a team led by Dr. Andrew Mendelian, professor of genomics at the University’s Department of Genetics and the director of the Genome Institute.
“I think the discovery is an important one that provides important information to help understand why we are suffering from arthritis and whether there is a genetic component to the disease,” Mendelic said.
“We think this gene plays a role in the development of inflammation in the joints.”
The researchers used a genetically modified mouse model that was genetically engineered to carry the mutation that caused the disorder and to be able to use this genetic information to create a mouse model of the disease.
The genetic information they used to create the mouse model allowed them to create an in vivo model of arthritis.
In a previous study, the scientists found that the mutation in the gene that causes arthritis is linked to a protein known as microglial activation.
The researchers found that microglia are activated in the body when a molecule called CpG dinucleotide-5 (CdG-5) is present in the cells of an animal.
This is why CdG is thought to cause inflammation.
CdGs are also known to play a role with cancer cells, but this is the first time that they have been linked to arthritis.
“It was exciting to find a gene involved in the disease that has been shown to be associated with inflammation and arthritis,” said lead author Dr. Steven A. Schaller, a professor of medicine and biostatistics at the Icahn School of Medicine at Mount Sinai in New York City.
The new study also found a gene in the mouse called CDK4 that was associated with arthritis in the mice. “
One of the things we have found is that Cdg5 is associated with the development and progression of arthritis, but we also found that it regulates inflammation and the response to inflammation in other cancers as well.”
The new study also found a gene in the mouse called CDK4 that was associated with arthritis in the mice.
Schillers research team found that CDK3, the gene for CDK2, is also associated with disease.
CDK6, the protein that controls the release of the inflammatory cytokine interleukin-6 (IL-6), was also linked to disease in the study.
“This gene has been implicated in the pathogenesis of a number of diseases,” said Schallers co-author Dr. Richard A. Himmelstein, a physician and director of UB’s Department for Cellular and Molecular Medicine.
“But we were also interested in looking at what was happening in other types of arthritis and finding out if the CDK gene might be associated.”
The team found a link between the mutation and inflammation in a mouse.
“The idea that CDG plays a crucial role in disease is exciting,” Schall.
“In mice, we were able to identify an interaction between the CDG gene and inflammatory mediators, like IL-6, that led to the formation of arthritis in a group of mice.”
The study has a number other exciting findings.
The mouse model showed the genetic mutation causes inflammation in three areas of the body, including the joints.
The mice also showed inflammation and inflammation-related diseases in their hearts.
Schilling said the mice were able get arthritis when they were in the first year of life.
“That was an exciting finding, especially in the presence of this mutation in mice,” Schill.
The research was funded by the National Institutes of Health, the Robert Wood Johnson Foundation, the University Health Network, the U.S. National Institutes on Aging, the Alzheimer’s Association, the Mayo Clinic and the Genomics Center at the Mayo Medical Center. “
As we get closer to a diagnosis for arthritis, we can hopefully start to use the mice in clinical trials to see if it can prevent or treat arthritis.”
The research was funded by the National Institutes of Health, the Robert Wood Johnson Foundation, the University Health Network, the U.S. National Institutes on Aging, the Alzheimer’s Association, the Mayo Clinic and the Genomics Center at the Mayo Medical Center.
The authors reported no conflicts of interest.