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MCF-7 breast cancer cells and HBL-100 breast epithelial cells were cultured with N-ethylmaleimide, a blocker of SH groups. Changes in redox potential of the glutathione system, activities of glutathione reductase, glutathione peroxidase, and intensity of apoptotic cell death were evaluated. The results indicate that incubation with N-ethylmaleimide led to glutathione system imbalance, reduced tumor cell redox potential, and induced their programmed death, which seemed useful for prospective target therapy of tumor diseases.

CD4(+) T cells orchestrate the immune response by differentiating into T helper (Th) or regulatory (Treg) cell subsets that secrete distinct sets of cytokines. They also play a critical role in the pathogenesis of autoimmunity, asthma, allergy and, likely, cancer. The mechanisms involved in the regulation of CD4(+) T cell homeostasis by galectin-1 remain poorly characterized. To investigate whether galectin-1 modulates the differentiation of CD4(+) T cells, the effects of galectin-1 on the mRNA expression levels of TBX21, GATA-3, FOXP3 and RORC in activated peripheral blood mononuclear cells were examined. The expression levels of GATA-3 and FOXP3 mRNA were up-regulated after treatment with 1.0 μg/ml galectin-1 and were unchanged (for GATA-3) or slightly elevated (for FOXP3) compared with untreated cells when 2.0 μg/ml galectin-1 was added. At the same time, at both concentrations of galectin-1, we observed reduced TBX21 and RORC mRNA expression levels. These findings support the concept that galectin-1 skews the differentiation of CD4(+) T cells towards Th2 and Treg cells.

Strontium ranelate (29 μg/ml) and ibandronic acid (50 μM) produced a cytotoxic effect on rat bone marrow myelokaryocytes in vitro. Strontium ranelate increased the number of myelokaryocytes with signs of necrosis, ibandronic acid increased the number of apoptotic and necrotic cells in the 9-day 2D culture of bone marrow cells on the plastic surface of the wells of culture plates. Co-culturing of the bone marrow with 3D matrices with microarc calcium phosphate coating that simulated bone mineral matrix increased intracellular ROS concentration, but abolished the cytotoxic effect of these drugs.

We studied the effect of galectin-1 on apoptosis of CD4(+) lymphocytes intact and in vitro differentiated towards regulatory T cells. An increase in the content of apoptotic CD4(+) lymphocytes was observed after exposure of intact cells with 15 ng/ml galectin-1 and after exposure of regulatory T cells with 10 and 15 ng/ml galectin-1. Apoptosis of regulatory T cells induced by galectin-1 was accompanied by an increase in the content of proapoptotic protein Bad.

We studied differentiation of multipotent mesenchymal stromal cells (MMSC) of the lungs of C57Bl/6 mice with bleomycin-induced pneumofibrosis. Adherent mononuclear cells found in mouse lungs demonstrated mesenchymal phenotype and expressed CD44, CD73, CD90, and CD106, but not CD31, CD34, and CD45. The cells with MMSC characteristics differentiate in vitro into various cells of stromal lines (chondrocytes, osteogenic cells, adipocytes, and fibroblasts). Bleomycin increased the growth rate of MMSC and selectively promoted their differentiation towards fibroblast cells.

Low-intensity ultrahigh frequency electromagnetic radiation (42 GHz, 100 microW/cm(2)) reduces the severity of inflammation and inhibits production of active oxygen forms by inflammatory exudate neutrophils only in mice with inflammatory process. These data suggest that some therapeutic effects of electromagnetic radiation can be explained by its antiinflammatory effect which is realized via modulation of functional activity of neutrophils in the focus of inflammation.