Joe E Springer, PhD

Mitochondrial Function, Inflammation, and microRNA (miRNA) Activity in Traumatic Brain Injury-
The goal of our research is to limit cell loss and the resulting neurological deficits following CNS injury by targeting steps occurring early in the cell death process. Recently, we have focused our efforts on identifying the mitochondrial events responsible for regulating cell survival and death following traumatic brain injury (TBI). Our most recent studies have revealed a novel role for mitochondria in the regulation of cellular miRNA activity and that TBI results in a intracellular compartmental shift of miRNAs regulating inflammation. Two of these inflammatory miRNAs are miR-146a and miR-223, which are known to affect myeloid cell phenotype by down-regulating pro-inflammatory markers while increasing expression markers of anti-inflammation. We are currently investigating nanocarrier-based cell delivery strategies to introduce inflammatory-related miRNA mimics/inhibitors to the injured brain as a way of targeting pro-inflammatory signaling and prompting reparative macrophage expression. These novel studies are being conducted by Wangxia Wang, Paresh Prajapati, Steven Pesina, and Urim Gelleta in collaboration with Pat Sullivan, John Gensel, and Adam Bachstetter.

Wang-Xia Wang, Ph.D., Research Assistant Professor

Paresh Prajapati, Ph.D., Lab Manager, Postdoctoral Scholar

Steven Pesina, Lab Tech, B.S. Chemistry

Urim Geleta, Neuroscience/Biology major