School of Medicine and Health Sciences Poster Presentations

Title

Endothelium derived factors influence differentiation of Fat derived MSCs

Document Type

Poster

Abstract Category

Obesity

Keywords

Endothelial cells, Mesenchymal stromal cells, adipogenic differentiation,

Publication Date

Spring 5-1-2019

Abstract

Fat derived mesenchymal stromal cells have a great potential for therapeutics due to its capability of tissue regeneration and ability to differentiate into several mature tissues such as bone, cartilage, muscle and fat. Metabolic diseases that influence energy expenditure or storage such as prediabetes and diabetes appear to influence the differentiation pathway and as a result also serve as an important biomarker. Cross talk between endothelium and adipose derived MSCs may play a crucial role in energy balance and insulin resistance, in situations such as exercise intervention in prediabetes or diabetes. Here, we investigated if endothelium derived paracrine properties or endothelial conditioned media can affect MSC differentiation in an adipogenic (obesinogenic) environment, such as prediabetes or diabetes. In vitro, commercially obtained mid passage (8 to 9) human fat-derived stromal cells were exposed to adipogenic media and endothelial conditioned media, ECM, (obtained from culturing mature endothelial cells, HUVECs, 40 fold concentrated) at 1:100 ratio (n=3). MSC differentiation was monitored by RT-PCR and effect on adipogenesis was further assessed by oil-red-O staining of intracellular lipid vacuoles. We noted a reduced expression of markers for adipogenic differentiation such as PL1N, FABP4, CEBPA and PPARG (24.6, 13.3, 9.8, 4.2 fold, p= 0.00001, 0.02, 0.00001, 0.0001 respectively). We also observed increased expression of bone formation markers RUNX2 and BMP2 (1.5, 1.3 fold, p=0.01, 0.01 respectively) which were increased significantly. We also noted upregulation of endothelial genes such as VEGF and KDR (1.6 and 2.3 fold, respectively). Oil-red-o staining showed reduced lipid droplets where endothelial condition media was added. We conclude that addition of ECM appear to reduce adipogenesis of mid-passage fat derived human MSCs while augmenting bone formation markers. These outcomes indicate a cross-talk between endothelium and adipose derived cells which may influence differentiation potential towards bone. Further studies are underway to identify specific proteins in ECM that prevents adipogenesis of MSCs in an adipogenic environment.

Open Access

1

Comments

Presented at Research Days 2019.

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Endothelium derived factors influence differentiation of Fat derived MSCs

Fat derived mesenchymal stromal cells have a great potential for therapeutics due to its capability of tissue regeneration and ability to differentiate into several mature tissues such as bone, cartilage, muscle and fat. Metabolic diseases that influence energy expenditure or storage such as prediabetes and diabetes appear to influence the differentiation pathway and as a result also serve as an important biomarker. Cross talk between endothelium and adipose derived MSCs may play a crucial role in energy balance and insulin resistance, in situations such as exercise intervention in prediabetes or diabetes. Here, we investigated if endothelium derived paracrine properties or endothelial conditioned media can affect MSC differentiation in an adipogenic (obesinogenic) environment, such as prediabetes or diabetes. In vitro, commercially obtained mid passage (8 to 9) human fat-derived stromal cells were exposed to adipogenic media and endothelial conditioned media, ECM, (obtained from culturing mature endothelial cells, HUVECs, 40 fold concentrated) at 1:100 ratio (n=3). MSC differentiation was monitored by RT-PCR and effect on adipogenesis was further assessed by oil-red-O staining of intracellular lipid vacuoles. We noted a reduced expression of markers for adipogenic differentiation such as PL1N, FABP4, CEBPA and PPARG (24.6, 13.3, 9.8, 4.2 fold, p= 0.00001, 0.02, 0.00001, 0.0001 respectively). We also observed increased expression of bone formation markers RUNX2 and BMP2 (1.5, 1.3 fold, p=0.01, 0.01 respectively) which were increased significantly. We also noted upregulation of endothelial genes such as VEGF and KDR (1.6 and 2.3 fold, respectively). Oil-red-o staining showed reduced lipid droplets where endothelial condition media was added. We conclude that addition of ECM appear to reduce adipogenesis of mid-passage fat derived human MSCs while augmenting bone formation markers. These outcomes indicate a cross-talk between endothelium and adipose derived cells which may influence differentiation potential towards bone. Further studies are underway to identify specific proteins in ECM that prevents adipogenesis of MSCs in an adipogenic environment.