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Cytometry A ; 95(1): 24-33, 2019 01.
Article in English | MEDLINE | ID: mdl-30240134

ABSTRACT

This study is aimed to reveal morphological and functional changes in multipotent mesenchymal stromal cells (MSCs) isolated from the rat bone marrow after: (i) activation of Toll-like receptors (TLRs) with teichoic acid (TA), (ii) impact on epidermal growth factor (EGF) receptors with activator EGF or inhibitor Herceptin, and (iii) treatment with DNA intercalator Cisplatin. According to our results, TA and EGF cause an increase in the synthesis of glycosaminoglycans, c-Myc content, and protein in the MSC cytoplasm. It was observed that the cell population in G0 phase decreased and the cell population in G1 phase increased, when compared with control. At the same time, the cell population with a higher nuclear-cytoplasmic ratio (NCR) in S and G2 phases also increased. This indicates the manifestation of the MSC mesenchymal phenotype, exhibiting indirect metabolic signs of the regenerative potential increase. In other experiments, Herceptin was shown to suppress only the stemness signs of MSCs, while Cisplatin seriously affected cell viability in general, reducing synthetic and proliferative activities and causing cell morphology disturbances. © 2018 International Society for Advancement of Cytometry.


Subject(s)
Cisplatin/pharmacology , Epidermal Growth Factor/pharmacology , Mesenchymal Stem Cells/cytology , Mesenchymal Stem Cells/metabolism , Animals , Bone Marrow Cells/chemistry , Bone Marrow Cells/cytology , Bone Marrow Cells/metabolism , Cell Differentiation/drug effects , Cell Proliferation/drug effects , Cell Survival/drug effects , Cells, Cultured , ErbB Receptors/agonists , ErbB Receptors/antagonists & inhibitors , Flow Cytometry , Glycogen/metabolism , Glycosaminoglycans/biosynthesis , Glycosaminoglycans/metabolism , Humans , Intercalating Agents/pharmacology , Male , Mesenchymal Stem Cells/chemistry , Proto-Oncogene Proteins c-myc/metabolism , Rats , Teichoic Acids/pharmacology , Toll-Like Receptors/metabolism , Trastuzumab/pharmacology
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