Dynamics of changes in the representation of mesenchymal cells in the forming glial scar during dexamethasone application

Mesenchymal stem cells are involved in cellular responses in the injured brain after a stroke. The formation of a glial scar is a local response in the brain to damage, and mesenchymal stem cells may be involved in the processes of scar formation. Mesenchymal stem cells express a range of membrane markers, the expression profile of which obviously changes as they differentiate and depends on the microenvironment in which these cells are located. However, it is still unclear where the stem cells in the damaged brain originate from – whether they come from a resident source or from the bone marrow, although an increase in CD34+ cells in the blood of stroke patients is a well-known fact. In this study, we consider the hypothesis regarding the appearance of mesenchymal stem cells in the brain during a stroke and their potential involvement in the formation of a glial scar. The aim of the study is to investigate the involvement of CD44+, CD68+, CD90+, and CD146+ cells in the formation of a glial scar during hemorrhagic stroke and the changes in their representation under the effect of dexamethasone. To achieve this goal, we simulated hemorrhagic stroke in rats and compared the results of immunohistochemical detection of CD44+, CD68+, CD90+, and CD146+ cells in the area of glial scar formation against the dexamethasone administration. We obtained convincing results of differences in the activity and timing of migration of cells expressing CD44 compared to cells expressing CD68, CD90, and CD146. There is a tendency indicating a dependence between the detection of CD44+ cells and the extent of the damage, while the detection of CD68+, CD90+, and CD146+ cells is strongly correlated and increases under the effect of dexamethasone. Cells expressing CD44 were the main participants in the infiltrating pool of cells in the acute phase, but dexamethasone delayed the peak accumulation of CD44+ cells in the forming scar. There were some changes in the detection of these cells around the hemorrhage during dexamethasone treatment, which may indicate its modulating effect on mesenchymal stem cells during glial scar formation. The more frequent detection of CD68+, CD90+, and CD146+ cells can be considered a manifestation of the potential modification by dexamethasone of cellular reactions involved in glial scar formation in the brain after a stroke. The study of the roles of specific immunophenotypes of mesenchymal stem cells in the areas of glial scar formation following hemorrhagic stroke opens new perspectives in the study of brain recovery processes.