A study published in the Journal of Neuroscience reportedly confirms the association between a variant in the gene FKBF5 and the level of pain people experience after a traumatic injury.
A 2013 study conducted by researchers at the University of North Carolina School of Medicine suggests that people with a variant or minor/risk allele on chromosome 6 known as rs3800373 are likely to experience more pain after exposure to trauma (such as sexual assault or motor vehicle collision) compared to people who don’t have this variant.
The recent study, conducted by the same researchers, confirms this association in a cohort of more than 1,500 people of both European American and African American descent who experienced motor vehicle collision trauma, explains a media release from University of North Carolina Health Care.
“In our current study, we showed that the reason this variant affects chronic pain outcomes is because it alters the ability of FKBP5 to be regulated by a microRNA called miR-320a,” says Sarah Linnstaedt, PhD, assistant professor of anesthesiology and an investigator in the Institute for Trauma Recovery, and the study’s lead author.
MicroRNAs play an important role in the regulation of gene expression, primarily by degrading or repressing the translation of messenger RNA (mRNA).
“In individuals with the minor/risk allele, the microRNA does not bind well to FKBP5,” she said. “In other words, it does not negatively regulate FKBP5, thus causing FKBP5 to be over-expressed. High levels of FKBP5 can be detrimental because it alters natural feedback mechanisms that control circulating cortisol (stress hormone) levels,” she adds.
Cortisol has been shown to directly sensitize peripheral nerves. Therefore, individuals with higher levels of this hormone (ie, individuals with the risk allele) are likely to experience more pain than individuals who do not have the risk allele, the release continues.
These results suggest certain therapeutic approaches that might be helpful, Linnstaedt states.
“I think it suggests we could use small molecules or inhibitor RNAs to decrease expression or inhibit activity of FKBP5, or we could use microRNA mimics to increase expression of the microRNA, miR-320a,” she says. “I could also imagine a gene editing approach that specifically changes the risk allele in FKBP5 to a protective allele.”
[Source(s): University of North Carolina Health Care, Science Daily]