Bone-Like Multilevel Calcium Phosphate Coating Modulates an Interaction of Mesenchymal Stem Cells and Tumor Cells

摘要

Modem biomaterial biocompatibility research focuses the biomaterial hierarchic effects on multipotent mesenchymal stromal cell (MMSC) behavior (that occur at the nano-, micro- and macroscales) because MMSCs are the fundamental units that produce/regenerate bone tissue. Leukemia initiation and progression are connected with a disfunction of health cell microenvironment and MMSCs. Continuous monitoring of MMSC and tumor cell interaction is a promising tool for oncology, cellular biology, biotechnology and environmental research. The aim was to investigate a modulation of in vitro interaction of human MMSCs and leukemic T lymphoblast-like cells (Jurkat T cells) caused by micro-arc multilevel calcium phosphate (CP) coating with the help of Cell-IQ and RTCA advanced tools for continuous monitoring. An average velocity of cell division (AVCD) of human adipose-derived MMSCs (hAMMSCs) contacted in vitro with allogenic Jurkat line of human leukemic T lymphoblasts (Jurkat T cells) was studied by means of Cell-IQ v2 MLF integrated phase-contrast microscopic platform for real-time surveillance imaging of living cells. Both 50 μL suspensions (5 ×10~4 viable karyocytes) of the CD73CD90CD105~+ adherent cells and Jurkat T cells were applied into the center of the well of 12-well plastic plates for 7 days at 100% humidity in a 5% CO_2 atmosphere at 37°C until a monolayer formation. A nutrient medium was once replaced. To determine cell invasion (chemotactic motility) through 8 μm pores the real-time cell analysis (RTCA DP Analyzer) with the CIM-plate was used. AVCD of fibroblast-like adherent hAMMSCs was 0.27-0.63 divisions/h. CP coating diminished significantly the percent of dividing hAMMSCs contacted with leukemic Jurkat T cells. RTCA system showed significant hAMMSC invasion towards tumor cells and not vice versa. For all this, cellular interaction led to increasing viability of Jurkat T cells and decreasing hAMMSC viability. Thus, tumor Jurkat T cells could control a fate of