Summary:
Multiple Sclerosis (MS) is an autoimmune disease that affects the Central
Nervous System (C.N.S.). The cause for this disease has not been fully
elucidated, because it presents a large genetic heterogeneity. Nevertheless, it
is clear that an immune response is provoked at the onset and during the
disease, that destroys the myelin sheath of nerve cells and, thus, blocks the
transmission of the nerve impulses. Due to heterogeneity, there is no unique
universal model for studying MS, but a variety of models that simulate the
different types of the disease. Among them, the most studied are the models of
Experimental Autoimmune Encephalomyelitis (Ε.Α.Ε.). In the present work, we
utilized Experimental Autoimmune Encephalomyelitis in the spinal cord of Mus
musculus. More specifically the pathway that produces inflammatory molecules
from arachidonic acid, such as prostaglandins, thromboxanes and leukotrienes
was studied. Therefore, the scientific research of this study focused on the
study of the superfamily of Phospholipases A2 (PLA2) and Cyclooxygenases. For
these enzymes, relative gene expression levels of fourteen PLA2 genes, as well
as those of COX-1 and COX-2, were determined by real time polymerase chain
reaction experiments, during three different time points of disease
progression. Moreover, a method based on lipidomic analysis with HPLC-MS/MS was
established in physiological brain and spinal cord tissues of Mus musculus.
Using this method, the substrates and the products of COX-2 and PLA2 will be
studied in the future. This will offer a more holistic view of the interactions
of lipid pathways, in which these enzymes are being implicated.
Keywords:
Phospholipases A2, Cyclooxygenases, Multiple Sclerosis, Experimental Autoimmune Encephalomyelitis
