Hemp Seed Oil Inhibits the Adipogenicity of the Differentiation-Induced Human Mesenchymal Stem Cells through Suppressing the Cannabinoid Type 1 (CB1).

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. This study compared the availability of phytocannabinoids [CBD and Δ9-tetrahydrocannabinol (THC)] and polyunsaturated fatty acids [omega 3 (ω3) and omega 6 (ω6)] in different hemp seed oils (HSO). The study also examined the effect of HSO on adipocyte lipid accumulation by suppressing cannabinoid receptors in adipogenesis-stimulated human mesenchymal stem cells (hMSCs). Most importantly, Oil-Red-O' and Nile red tests showed that HSO induced adipogenic hMSC differentiation without differentiation agents. Additionally, HSO-treated cells showed increased peroxisome proliferator-activated receptor gamma (PPARγ) mRNA expression compared to controls (hMSC). HSO reduced PPARγ mRNA expression after differentiation media (DM) treatment. After treatment with HSO, DM-hMSCs had significantly lower CB1 mRNA and protein expressions than normal hMSCs. HSO treatment also decreased transient receptor potential vanilloid 1 (TRPV1), fatty acid amide hydrolase (FAAH), and monoacylglycerol lipase (MGL) mRNAs in hMSC and DM-hMSCs. HSO treatment significantly decreased CB1, CB2, TRPV1, and G-protein-coupled receptor 55 (GPCR55) protein levels in DM-hMSC compared to hMSC in western blot analysis. In this study, HSO initiated adipogenic differentiation in hMSC without DM, but it suppressed CB1 gene and protein expression, potentially decreasing adipocyte lipid accumulation and lipogenic enzymes.

Decidua Parietalis Mesenchymal Stem/Stromal Cells and Their Secretome Diminish the Oncogenic Properties of MDA231 Cells In Vitro.

Mesenchymal 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. MDA231 cells were exposed to DPMSCs, and their biological functions, including adhesion, proliferation, migration, and invasion, were evaluated. In addition, genomic and proteomic modifications of the MDA231 cell line, in response to the DPMSCs, were also evaluated. MDA231 cells exhibited a significant reduction in proliferation, migration, and invasion potential after their treatment with DPMSCs. Furthermore, DPMSC treatment diminished the angiogenic potential of MDA231 cells. DPMSC treatment modulated the expression of various pro-apoptotic as well as oncogenes in MDA231 cells. The properties of DPMSCs to inhibit the invasive characteristics of MDA231 cells demonstrate that they may be a useful candidate in a stem-cell-based therapy against cancer.

Human Decidua Basalis mesenchymal stem/stromal cells reverse the damaging effects of high level of glucose on endothelial cells in vitro.

Recently, 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 (H2 O2 ) and monocytes. In addition, DBMSCs induce the generation of anti-cancer immune cells known as M1 macrophages. Diabetes is another inflammatory disease where endothelial cells are injured by H2 O2 produced by high level of glucose (hyperglycaemia), which is associated with development of thrombosis. Here, we investigated the ability of DBMSCs to reverse the damaging effects of high levels of glucose on endothelial cells. DBMSCs and endothelial cells were isolated from human placental and umbilical cord tissues, respectively. Endothelial cells were incubated with glucose in presence of DBMSCs, and their functions were evaluated. The effect of DBMSCs on glucose- treated endothelial cell expression of genes was also determined. DBMSCs reversed the effects of glucose on endothelial cell functions including proliferation, migration, angiogenesis and permeability. In addition, DBMSCs modified the expression of several genes mediating essential endothelial cell functions including survival, apoptosis, permeability and angiogenesis. We report the first evidence that DBMSCs protect the functions of endothelial cells from the damaging effects of glucose. Based on these results, we establish that DBMSCs are promising therapeutic agents to repair glucose-induced endothelial cell injury in diabetes. However, these finding must be investigated further to determine the pathways underlying the protective role of DBMSCs on glucose-stimulated endothelial cell Injury.

Correction to: Preconditioning of Human Decidua Basalis Mesenchymal Stem/Stromal Cells with Glucose Increased Their Engraftment and Anti-diabetic Properties.

The author would like to correct the names for the below co-authors in the online published article.

Preconditioning of Human Decidua Basalis Mesenchymal Stem/Stromal Cells with Glucose Increased Their Engraftment and Anti-diabetic Properties.

BACKGROUND: 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 (H2O2) and immune cells. Here, we studied the consequences of glucose, another oxidative stress inducer, on the phenotypic and functional changes in DBMSCs. METHODS: DBMSCs were exposed to a high level of glucose, and its effect on DBMSC phenotypic and functional properties was determined. DBMSC expression of oxidative stress and immune molecules after exposure to glucose were also identified. RESULTS: Conditioning of DBMSCs with glucose improved their adhesion and invasion. Glucose also increased DBMSC expression of genes with survival, proliferation, migration, invasion, anti-inflammatory, anti-chemoattractant and antimicrobial properties. In addition, DBMSC expression of B7H4, an inhibitor of T cell proliferation was also enhanced by glucose. Interestingly, glucose modulated DBMSC expression of genes involved in insulin secretion and prevention of diabetes. CONCLUSION: These data show the potentially beneficial effects of glucose on DBMSC functions. Preconditioning of DBMSCs with glucose may therefore be a rational strategy for increasing their therapeutic potential by enhancing their engraftment efficiency. In addition, glucose may program DBMSCs into insulin producing cells with ability to counteract inflammation and infection associated with diabetes. However, future in vitro and in vivo studies are essential to investigate the findings of this study further.