Central and peripheral mechanisms of the endocannabinoid system (ECS) favor energy intake and storage. The ECS, especially cannabidiol (CBD) receptors, controls adipocyte differentiation (hyperplasia) and lipid accumulation (hypertrophy) in adipose tissue. In white adipose tissue, cannabidiol receptor 1 (CB1) stimulation increases lipogenesis and inhibits lipolysis; in brown adipose tissue, it decreases mitochondrial thermogenesis and biogenesis.
View Article and Find Full Text PDFMesenchymal stem cells (MSCs) have been shown to suppress tumor growth, inhibit angiogenesis, regulate cellular signaling, and induce apoptosis in cancer cells. We have earlier reported that placenta-derived decidua parietalis mesenchymal stem/stromal cells (DPMSCs) not only retained their functional characteristics in the cancer microenvironment but also exhibited increased expression of anti-apoptotic genes, demonstrating their anti-tumor properties in the tumor setting. In this study, we have further evaluated the effects of DPMSCs on the functional outcome of human breast cancer cell line MDA231.
View Article and Find Full Text PDFRecently, we reported the therapeutic potential of mesenchymal stem/stromal cells (MSCs) from the maternal decidua basalis tissue of human term placenta (DBMSCs) to treat inflammatory diseases, such as atherosclerosis and cancer. DMSCs protect endothelial cell functions from the negative effects of oxidative stress mediators including hydrogen peroxide (H O ) and monocytes. In addition, DBMSCs induce the generation of anti-cancer immune cells known as M1 macrophages.
View Article and Find Full Text PDFThe author would like to correct the names for the below co-authors in the online published article.
View Article and Find Full Text PDFBackground: Mesenchymal stem/stromal cells (MSCs) from the decidua basalis (DBMSCs) of the human placenta have important functions that make them potential candidates for cellular therapy. Previously, we showed that DBMSC functions do not change significantly in a high oxidative stress environment, which was induced by hydrogen peroxide (HO) and immune cells. Here, we studied the consequences of glucose, another oxidative stress inducer, on the phenotypic and functional changes in DBMSCs.
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