Induced osteogenesis of mesenchymal stem cells (MSCs) may provide an important tool for bone injuries treatment. Human umbilical cord and adipose tissue are routinely discarded as clinical waste and may be used as noncontroversial MSCs sources. It still remains to be verified which source of MSCs is the most suitable for bone regeneration. The aim of this research was to investigate the osteogenic potential of human MSCs derived from adipose tissue (AT-MSCs) and Wharton's jelly of the human umbilical cord (WJ-MSCs) differentiated under the same conditions. Osteogenic differentiation of MSCs was detected and quantified by alizarin red S (ARS) staining for calcium deposition and alkaline phosphatase (ALP) activity, osteoprotegerin (OPG), and osteocalcin (OC) secretion measurements. Under osteogenic conditions, after 21 days of differentiation, the measured ALP activity and calcium deposition were significantly higher in the AT-MSCs than in the WJ-MSCs, while the OPG and OC secretion were higher in the WJ-MSCs vs. AT-MSCs. Low concentrations of OPG and high levels of OC in AT-MSCs and WJ-MSCs, prove that these cells reached an advanced stage of the osteogenic differentiation. The levels of OC secreted by AT-MSCs were lower than by WJ-MSCs. Both cell types, AT-MSCs and WJ-MSCs possess a potential to differentiate towards the osteogenic lineage. The observed differences in the levels of osteogenic markers suggest that after 21-days of osteogenic differentiation, the AT-MSCs might have reached a more advanced stage of differentiation than WJ-MSCs.

Clinical and epidemiological studies show that docosahexaenoic acid (DHA) and arachidonic acid (AA) exert multiple effects on ovarian cancer. While DHA seems to inhibit growth and prevent carcinogenic processes, stimulation of leukotriene B4 receptors BLT1 and BLT2 by several eicosanoids derived from AA plays an important role in mediating cisplatin resistance in ovarian cancer cells. We examined whether DHA and AA exerted antiproliferative effect on epithelial ovarian cancer cells and whether these polyunsaturated fatty acids could alter their susceptibility to cisplatin. Using SKOV3 and OVCAR3 cell lines, we found that DHA but not AA suppressed the cells viability, proliferation, enhanced cell death, and induced activation of caspase-3/7 in the concentration- and time-dependent manner. The OVCAR3 cells were less susceptible to cisplatin than SKOV3 cells. DHA but not AA significantly potentiated cisplatin cytotoxicity in SKOV3 and OVCAR3 cells. We did not observe any significant influence of AA on the above mentioned processes in both cell lines. Similar effect can occur in ovarian cancer patients treated with cisplatin and supplemented with DHA.