Dmitry KashirskikhInstitute of General Pathology and Pathophysiology, Russian Federation
Title: In vivo LDL desialylation model
Objectives: It has been considered that the initial link in atherogenesis is a modification of LDL. One of the types of atherogenic modification is the LDL desialylation. The aim of this study was to model the LDL desialylation in vivo. Administration of a fixed concentration of neuraminidase immobilized on IgG would allow us to model the desialylation of LDL revealed in humans.
Materials and Methods: The control group of C57BL6 mice (n=48) was treated by a single injection of saline, while the experimental group (n=48) received Vibrio Cholerae neuraminidase conjugated with mouse IgG. Mice were terminated at fixed periods: before and after a single injection (1-7 days). LDL was isolated from serum by ultracentrifugation. The content of sialic acid was determined according to Warren’s method. Lipids of serum were measured by commercial kits.
Results: A significant decrease in LDL sialic acid by 30% was detected up to 5 days after the neuraminidase injection. Also, serum levels of triglycerides, total cholesterol and HDL-cholesterol in experimental mice did not differ compared with wild-type control mice.
Conclusions: LDL desialylation has been successfully modeled in vivo. In addition, LDL desialylation did not affect blood lipid levels in mice. It is needed to do further research on the effect of LDL desialylation using a high fat diet and transgenic mice (ApoE-/- or Ldlr-/-).
Dmitry Kashirskikh is a junior researcher at the Laboratory of Cellular and Molecular Pathology of Cardiovascular System, Avtsyn Research Institute of Human Morphology of Federal state budgetary scientific institution "Petrovsky National Research Centre of Surgery" (Moscow, Russian Federation). He received a grant from the Russian Science Foundation (22-25-00391) for the study of atherosclerosis. Also, he is a member of the European Atherosclerosis Society (EAS). His areas of interest includes atherogenic LDL modifications, deglycosylation in atherosclerosis and mitochondrial DNA mutations in atherosclerosis.