Purdue University researchers have discovered miR-199 (a type of “microRNA), a genetic molecule, which reduces the migration of neutrophils and hence possibly relieve inflammation without compromising the immune system. This is an important potential breakthrough because current medications that mitigate inflammation cause a variety of diseases such as rheumatic arthritis as well as potentially compromise the patient’s immune system. The Purdue team discovery may open up a new approach to target inflammation.
This breakthrough may work by alleviating inflammation by suppressing the migration of neutrophils, a type of white blood cell. These cells migrate within tissues to kill pathogens but also trigger excessive inflammation causing tissue injury and other adverse effects, reported Emil Venere from the Purdue Newsroom.
miR-199: A New Breakthrough
A type of microRNA, it can reduce the migration of neutrophils and hence possibly reduce inflammation without adversely impacting the immune system. microRNAs have been used in clinical trials recently to treat cancer and infection. Additionally, they are leveraged as screening tools for the identification of underlying mechanisms of diseases and cell behavior.
Importantly, the researchers claim that the role of microRNAs for the regulation of neutrophil migration was largely unknown.
The team capitalized on genetic-screening methods to identify eight microRNAs that are involved with the suppression of neutrophilic migration—including miR-199. The team uncovered that miR-199 suppresses the action of cyclin-dependent kinase 2 (CDK2), an enzyme—and hence impacting the migration of neutrophils. The Purdue led researchers uncovered that CDK2’s link to neutrophil migration was not known according to recent press. The preclinical research was conducted in zebrafish and in human neutrophil-like cells in a laboratory.
One of the research leads, Qing Deng, assistant professor in the Department of Biological Sciences, Purdue University, reported, “This work suggests miR-199 and CDK2 could be new targets for treating inflammatory ailments and introduces an avenue of the function for CDK2 outside the cell cycle regulation.”
Findings of this study are detailed online in the Proceedings of the National Academy of Sciences.
Alan Y. Hsu, doctoral student, Purdue Department of Biological Sciences
Qing Deng, assistant professor in the Department of Biological Sciences, Purdue University
Other groups involved include:
· Medical College of China Three Gorges University, Institute of Infection and Inflammation
· Indiana University School of Medicine, Department of Medical and Molecular Genetics and Center for Computational Biology and Bioinformatics
Call to action: This work is ongoing and the team’s next step involves the understanding of the detailed molecular mechanisms for how CDK2 suppresses neutrophil migration and lethal inflammation. Research lead Qing Deng can be contacted at firstname.lastname@example.org. TrialSite News will monitor this research group and offer updates to our network.