Surya Sanjay
Pronouns: he/him/his
Research Mentor(s): Lloyd Ruiz
Co-Presenter:
Research Mentor School/College/Department: Molecular & Integrative Physiology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 1 – 10am – 10:50am
Room: League Ballroom
Authors:
Presenter: 90
Abstract
Aging leads to the fragmentation and dysfunction of the neuromuscular junction (NMJ), which further impairs neuromuscular communication and muscle contraction, while also contributing to muscle atrophy. Although the function of myonuclei that accumulate and localize at the NMJ, known as subsynaptic myonuclei, is unknown, previous literature has suggested that they are connected with the gene regulation of proteins responsible for maintaining synaptic architecture. It has also been observed that NMJs in aged mice contain fewer subsynaptic myonuclei and that the knock-out of the LMNA gene seems to accelerate NMJ degeneration and reduce the number of myonuclei confined to the endplate. As a result, this study aimed to examine and characterize subsynaptic myonuclei, as well as their role in NMJ degeneration. Parallel quantitative polymerase chain reactions (qPCR) and immunohistochemistries (IHC) were run on primary muscle cells isolated from mice (1) without, (2) three days after, and (3) seven days after sciatic nerve transection (SNT), a surgical procedure thought to act as a proxy for aging. Analyses demonstrated that SNT led to a 13-fold increase of LMNA RNA, and there was no significant (p < 0.05) change in the number of subsynaptic myonuclei. Presentation link
Biomedical Sciences
