COBRE for the Center for Molecular Medicine: Scope- Role of MK2 Following Traumatic Brain Injury

This 2-year pilot award will generate preliminary data investigating the role of MAPK-activated protein kinase 2 (MK2) following traumatic brain injury (TBI). Despite multiple attempts no drug has earned FDA approval for TBI. Control of neuroinflammation is a promising avenue to achieve neuroprotection and improve patient outcomes. Still, there is an urgent need to identify the molecular mechanisms that regulate inflammation, so selective therapeutic agents can be developed. Our prior work has demonstrated that the mitogen-activated protein kinases (MAPK) pathway is involved in detrimental neuroinflammation following injury or in neurodegenerative disease [1-4]. From our prior work we have recently identified the protein MK2, which we postulate maybe an enzyme specific to the detrimental proinflammatory response to TBI. Using a mild closed head injury model in mice we will address our overall hypothesis: MK2 deficiency will prevent TBI induced neurological deficits. If successful, we will have identified a novel therapeutic target that regulates neuroinflammation following TBI, which will lay the foundation to garner NIH funding to explore the pathway in greater detail.