Investigation of expression levels of LGR4 and CTSH genes in the RANK pathway in the Myasthenia Gravis Mouse Model.

Myasthenia Gravis (MG) is a weakened muscle disease with autoimmune based. Autoantibodies bind to the antigenic structures in which they develop, causing morphological and functional changes in the postsynaptic membrane, and then neuromuscular conduction disorder and muscle weakness occur. The RANK pathway is a pathway that includes functions such as the differentiation of osteoblasts, the main cells of bones, into osteoclasts. Binding of RANK to its ligand, RANKL, affects dendritic cell viability, apoptosis, and the capacity to stimulate the immune system. There are studies showing that some genes in the RANK pathway are associated with autoimmune diseases. In this study, it was aimed to examine the expression levels of LGR4 and CTSH genes, which are known to be based on the RANK pathway and play a role in many autoimmune diseases, in an experimental autoimmune MG (DOMG) mouse model. Evaluated mouse lymph ganglia cells are samples of mice used in the previous project (Project No: TYL-2017-27428), stored in liquid nitrogen. Total lymph ganglion cells from female mice (n=4) immunized with torpedo AChR, an antibody specific for MG disease, were used as the experimental group, and total lymph ganglion cells from female mice (n=4) injected with Complete Freud's Adjuvant's (CFA) were used as the control group. Gene expression levels were determined by RT-PCR and compared between groups. In DOMG modeled mice, compared to the control group; It was observed that LGR4 expression levels tended to decrease (p=0.8846), while CTSH expression levels showed a tendency to increase (p=0.6857). The decrease in LGR4 expression level and the increase in CTSH expression level in the DOMG group were not statistically significant. This is the first study conducted on DOMG mice to determine the role of LGR4 and CTSH in the pathogenesis of the disease, and more detailed analyzes are needed.