Dataset Information

Evaluating the effect of arachidonic acid and eicosapentaenoic acid on induction of adipogenesis in human adipose-derived stem cells.

ABSTRACT: Objectives:Adipose tissue is one of the most important endocrine organs that liberates many metabolic mediators such as hormones, cytokines, and chemokines. Different types of fatty acids have key roles in adipogenesis. The aim of this study was to evaluate the effects of two essential fatty acids, including Arachidonic acid (AA) and Eicosapentaenoic acid (EPA), on the process of adipogenicity in human Adipose-Derived Stem Cells (hADSCs). Materials and Methods:After immunophenotyping of hADSCs by flowcytometry, they were differentiated into adipocytes and simultaneously exposed to 30 ?M and 60 ?M of AA and 25 ?M and 50 ?M of EPA. Further, along with the MTS assay, the activity of glycalaldehyde-3-phosphate dehydrogenase (GAPDH) was also measured. In addition, expression of lipid markers including peroxisome proliferator-activated receptor ?2 (PPAR?2) and glucose transporter 4 (GLUT4) was evaluated, and the neutral lipid contents were determined using Oil red O staining. Results:MTS evaluation showed a significant decrease in proliferation in all treatment groups compared to the control group. Based on oil red O staining, fat droplets in the AA treatment groups were higher than in controls. The expression of PPAR?2 and GLUT4 genes and proteins increased in almost all AA and EPA groups compared to control. In addition, GAPDH activity was higher in AA groups than in the control group. In general, while different concentrations of EPA did not increase the adipogenic process compared to the control group, stimulation of differentiation to adipocytes was largely determined by the AA. Conclusion:The result indicates a positive effect of omega-6 versus omega-3 in stimulating the pathways of adipogenesis.

SUBMITTER: Mostoli R

PROVIDER: S-EPMC7478257 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Evaluating the effect of arachidonic acid and eicosapentaenoic acid on induction of adipogenesis in human adipose-derived stem cells.

Mostoli Rezvan R Goudarzi Farjam F Mohammadalipour Adel A Khodadadi Iraj I Goodarzi Mohammad Taghi MT

Iranian journal of basic medical sciences 20200801 8

<h4>Objectives</h4>Adipose tissue is one of the most important endocrine organs that liberates many metabolic mediators such as hormones, cytokines, and chemokines. Different types of fatty acids have key roles in adipogenesis. The aim of this study was to evaluate the effects of two essential fatty acids, including Arachidonic acid (AA) and Eicosapentaenoic acid (EPA), on the process of adipogenicity in human Adipose-Derived Stem Cells (hADSCs).<h4>Materials and methods</h4>After immunophenotyp ...[more]

PMID: 32952949

Similar Datasets

Project description:Salmons raised in aquaculture farms around the world are increasingly subjected to sub-optimal environmental conditions, such as high water temperatures during summer seasons. Aerobic scope increases and lipid metabolism changes are known plasticity responses of fish for a better acclimation to high water temperature. The present study aimed at investigating the effect of high water temperature on the regulation of fatty acid metabolism in juvenile Atlantic salmon fed different dietary ARA/EPA ratios (arachidonic acid, 20:4n-6/ eicosapentaenoic acid, 20:5n-3), with particular focus on apparent in vivo enzyme activities and gene expression of lipid metabolism pathways. Three experimental diets were formulated to be identical, except for the ratio EPA/ARA, and fed to triplicate groups of Atlantic salmon (Salmo salar) kept either at 10°C or 20°C. Results showed that fatty acid metabolic utilisation, and likely also their dietary requirements for optimal performance, can be affected by changes in their relative levels and by environmental temperature in Atlantic salmon. Thus, the increase in temperature, independently from dietary treatment, had a significant effect on the β-oxidation of a fatty acid including EPA, as observed by the apparent in vivo enzyme activity and mRNA expression of pparα -transcription factor in lipid metabolism, including β-oxidation genes- and cpt1 -key enzyme responsible for the movement of LC-PUFA from the cytosol into the mitochondria for β-oxidation-, were both increased at the higher water temperature. An interesting interaction was observed in the transcription and in vivo enzyme activity of Δ5fad-time-limiting enzyme in the biosynthesis pathway of EPA and ARA. Such, at lower temperature, the highest mRNA expression and enzyme activity was recorded in fish with limited supply of dietary EPA, whereas at higher temperature these were recorded in fish with limited ARA supply. In consideration that fish at higher water temperature recorded a significantly increased feed intake, these results clearly suggested that at high, sub-optimal water temperature, fish metabolism attempted to increment its overall ARA status -the most bioactive LC-PUFA participating in the inflammatory response- by modulating the metabolic fate of dietary ARA (expressed as % of net intake), reducing its β-oxidation and favouring synthesis and deposition. This correlates also with results from other recent studies showing that both immune- and stress- responses in fish are up regulated in fish held at high temperatures. This is a novel and fundamental information that warrants industry and scientific attention, in consideration of the imminent increase in water temperatures, continuous expansion of aquaculture operations, resources utilisation in aquafeed and much needed seasonal/adaptive nutritional strategies.

Project description:Introduction:Adipose-derived stromal/stem cells (ASCs) have attracted attention as a promising material for regenerative medicine. Previously, we reported an age-related decrease in the adipogenic potential of ASCs from human subjects and found that the individual difference in this potential increased with age, although the mechanisms remain unclear. Recently, other groups demonstrated that a secreted antagonist of bone morphogenetic protein (BMP) signaling, Gremlin 2 (GREM2), inhibits the differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) into osteoblasts and the adipogenesis of 3T3-L1 cell. Here, we examined the effects of GREM2 on the differentiation of ASCs into adipocytes. Methods:To examine changes in GREM2 expression levels with age, immunohistochemistry was performed on subcutaneous adipose tissues from subjects 12-97 years of age. Next, GREM2 gene expression levels in ASCs collected from subjects 5-90 years of age were examined by RT-PCR, and the change with age and correlation between the expression level and the adipogenic potential of ASCs were analyzed. In addition, to assess whether GREM2 affects adipogenesis, ASCs (purchased from a vendor) were cultured to induce adipogenesis with recombinant GREM2 protein, and siRNA-induced GREM2 knockdown experiment was also performed using aged ASCs. Results:In adipose tissues, GREM2 expression was observed in cells, including ASCs, but not in mature adipocytes, and the expression level per cell increased with age. GREM2 expression levels in ASCs cultured in vitro also increased with age, and the individual differences in the level increased with age. Of note, partial correlation analysis controlled for age revealed that the adipogenic potential of ASCs and the GREM2 gene expression level were negatively correlated. Furthermore, based on a GREM2 addition experiment, GREM2 has inhibitory effects on the adipogenesis of ASCs through activation of Wnt/?-catenin signaling. On the other hand, GREM2 knockdown in aged ASCs promoted adipogenesis. Conclusions:The GREM2 expression level was confirmed to play a role in the age-related decrease in adipogenic potential observed in ASCs isolated from adipose tissues as well as in the enhancement of the individual difference, which increased with age. GREM2 in adipose tissues increased with age, which suggested that GREM2 functions as an inhibitory factor of adipogenesis in ASCs.

Project description:BackgroundThe clinical features of keloids consist of aberrant proliferation, secretion, differentiation and apoptosis of keloid dermis-derived fibroblasts (KFBs). Notably, the apoptosis rate of KFBs is lower than the proliferation rate. Though the anti-fibrotic effect of adipose-derived stem cells (ADSCs) on keloids has become a hot topic of research, the exact anti-fibrotic mechanism of the paracrine effect remains unclear. This study aimed to find out how the conditioned medium of ADSCs (ADSC-CM) exerts an anti-fibrotic effect in KFBs.MethodsKFBs and ADSCs were extracted and cultured. Then, ADSC-CM was prepared. Whether ADSC-CM could inhibit KFB growth and induce apoptosis was verified by the use of a cell counting kit-8, an 5-Ethynyl-2-deoxyuridine (Edu) kit and flow cytometry. The expressions of cyclooxygenase-1 (COX-1), COX-2, caspase 3 and B-cell lymphoma-2 (Bcl-2) in ADSC-CM-cultured KFBs were tested by real-time PCR and western blotting. To clarify the role of COX-2 in ADSC-CM-induced KFB apoptosis, a specific COX-2 inhibitor, celecoxib, was applied to KFBs cultured in ADSC-CM. Moreover, we tested the production of arachidonic acid (AA) and prostaglandin E2 (PGE2) by ELISA. Then, we established a keloid transplantation model in a nude mouse to validate the therapeutic effect in vivo.ResultsThe proliferation ability of KFBs cultured in ADSC-CM was found to be weakened and apoptosis was significantly increased. Caspase 3 expression was significantly upregulated and Bcl-2 was downregulated in ADSC-CM-cultured KFBs. Furthermore, ADSC-CM strikingly elevated COX-2 mRNA and protein expressions, but COX-1 expression was unaltered. COX-2 inhibitors reduced ADSC-CM-induced apoptosis. Additionally, COX-2 inhibition blocked the elevation of caspase 3 and reversed the decrease in Bcl-2 expression. ADSC-CM increased PGE2 levels by 1.5-fold and this effect was restrained by COX-2 inhibition. In the nude mouse model, expressions of AA, COX-2 and PGE2 were higher in the translated keloid tissues after ADSC-CM injection than in the controls.ConclusionsWe showed activation of the COX-2/PGE2 cascade in KFBs in response to ADSC-CM. By employing a specific COX-2 inhibitor, COX-2/PGE2 cascade activation played a crucial role in mediating the ADSC-CM-induced KFB apoptosis and anti-proliferation effects.

Dataset Information

Evaluating the effect of arachidonic acid and eicosapentaenoic acid on induction of adipogenesis in human adipose-derived stem cells.

Publications

Evaluating the effect of arachidonic acid and eicosapentaenoic acid on induction of adipogenesis in human adipose-derived stem cells.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets