New research published ahead of print in the journal Function finds that traumatic brain injury (TBI) disrupts inward-rectifier potassium channel function to cause system-wide vascular dysfunction.
Inward-rectifier potassium channels play an important role in blood flow and relies on phosphatidylinositol 4,5-bisphosphate (PIP2) to work properly. PIP2 is a component of cell membranes that is involved with a variety of cell functions and is depleted when inflammation is present.
Post-trauma inflammation has been shown to cause blood clotting disorders, vascular leaks and other problems associated with the endothelium, the lining of the blood vessels. In a new study, researchers analyzed a rat model of TBI to identify signaling pathways associated with PIP2.
“Collectively, our results support a novel mechanism to explain endotheliopathy in trauma, through diminished [inward-rectifier potassium channel] responses which can be rescued by PIP2. These findings may be generalizable to other pathological conditions characterized by altered lipid metabolism pathways and reductions in PIP2 levels, and suggest PIP2 may be a potential therapeutic target to improve endothelial function in conditions characterized by altered lipid metabolism such as brain trauma and stroke,” the research team wrote.
Read the full article, “Traumatic brain injury impairs systemic vascular function through disruption of inward-rectifier potassium channels.” Contact the APS Communications Office to schedule an interview with the research team.
