VCOM Research Day Program Book 2023

Medical Student Research Biomedical

07 Remyelination of Injured Peripheral Nerves in NANOG Infused Mice

Reilly Ellis; Carey Hung; Gabriella Kayal; Pihu Mehrotra; Kirkwood Personius; Kelly C.S. Roballo, DMV, PhD Corresponding author: Rellis01@vcom.edu; chung@vcom.edu; gkayal@vcom.edu

Edward Via College of Osteopathic Medicine-Virginia Campus University of Buffalo

Myelin insulates axons to facilitate rapid signal conductance of neuronal impulses to the brain and further to muscles. Peripheral nerve injuries (PNI) sever neuronal axons causing decreased signal transduction through myelin degeneration and denervation of muscle fibers leading to muscle atrophy. Exogenous application of NANOG, a transcription factor critical for embryonic and fetal development through maintenance of embryonic stem cell pluripotency, has the capacity to reverse maturation of adult myocytes for potential regeneration. However, its regenerative effects on myelin have not yet been investigated. This study explores NANOG’s effects on injured nerves and hypothesizes the addition of NANOG in vivo to injured peripheral nerves will increase the regeneration of myelin. We have two groups: Wild

type and NANOG-treated adult mice (n=24). Each mouse has an injured right nerve with a corresponding uninjured left nerve, with exception of two wild type mice who only received nerve injuries. Samples of these nerves were extracted at 5 weeks and 16 weeks post-nerve injury. All nerves are stained with Fluoromyelin, a compound that specifically adheres to myelin, and imaged under a fluorescent microscope. Images are uploaded to an Image J program that measures the mean grey value, which indicates the concentration of fluorescence in each image. This represents post-nerve injury myelin quantity. Current analysis is ongoing; however, results are displaying increases in myelin quantity of injured mice who received NANOG compared to the injured wild-type group at 5- and 16-weeks post-injury. These findings suggest that local application of NANOG to PNI

can facilitate remyelination of injured axons. Future research should investigate NANOG’s capacity to guide regeneration of functional synapses at the neuromuscular junction to elicit recovery of muscle contraction close to pre-injury strength. Nevertheless, the results of this study provide intriguing potential future clinical applications of NANOG as treatment for PNIs involving hypotonia and sensorimotor deficits, or other demyelinating diseases.

62