Dataset Information

FATP1 Exerts Variable Effects on Adipogenic Differentiation and Proliferation in Cells Derived From Muscle and Adipose Tissue.

ABSTRACT: In livestock, intramuscular adipose tissue is highly valued whereas adipose tissue in other depots is considered as waste. Thus, genetic factors that favor fat deposition in intramuscular compartments over that in other adipose depots are highly desirable in meat-producing animals. Fatty acid transport 1 (FATP1) has been demonstrated to promote cellular fatty acid uptake and metabolism; however, whether it also influences cellular lipid accumulation remains unclear. In the present study, we investigated the effects of FATP1 on the differentiation and proliferation of adipocytes in five types of cells derived from muscle and adipose tissue and estimated the effects of FATP1 on intramuscular fat (IMF) deposition. We showed that FATP1 is mainly expressed in heart and muscle tissue in buffaloes as well as cells undergoing adipogenic differentiation. Importantly, we found that FATP1 promoted the adipogenic differentiation of muscle-derived cells (buffalo myocytes and intramuscular preadipocytes and mouse C2C12 cells) but did not affect, or even inhibited, that of adipose-derived cells (buffalo subcutaneous preadipocytes and mouse 3T3-L1 cells, respectively). Correspondingly, our results further indicated that FATP1 promotes IMF deposition in mice in vivo. Meanwhile, FATP1 was found to enhance the proliferative activity of all the assessed cells, except murine 3T3-L1 cells. These results provide new insights into the potential effects of FATP1 on IMF deposition, especially regarding its positive effects on meat quality in buffaloes and other livestock.

SUBMITTER: Huang J

PROVIDER: S-EPMC9310014 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Mesenchymal stem cells (MSCs) are multipotent cells able to differentiate into multiple cell types, including adipocytes, osteoblasts, and chondrocytes. The role of adipose-derived stem cells (ADSCs) in cancers is significantly relevant. They seem to be involved in the promotion of tumour development and progression and relapse processes. For this reason, investigating the effects of breast cancer microenvironment on ADSCs is of high importance in order to understand the relationship between tumour cells and the surrounding stromal cells. With the current study, we aimed to investigate the specific characteristics of human ADSCs isolated from the adipose tissue of breast tumour patients. We compared ADSCs obtained from periumbilical fat (PF) of controls with ADSCs obtained from adipose tissue of breast cancer- (BC-) bearing patients. We analysed the surface antigens and the adipogenic differentiation ability of both ADSC populations. C/EBPδ expression was increased in PF and BC ADSCs induced to differentiate compared to the control while PPARγ and FABP4 expressions were enhanced only in PF ADSCs. Conversely, adiponectin expression was reduced in PF-differentiated ADSCs while it was slightly increased in differentiated BC ADSCs. By means of Oil Red O staining, we further observed an impaired differentiation capability of BC ADSCs. To investigate this aspect more in depth, we evaluated the effect of selective PPARγ activation and nutritional supplementation on the differentiation efficiency of BC ADSCs, noting that it was only with a strong differentiation stimuli that the process took place. Furthermore, we observed no response in BC ADSCs to the PPARγ inhibitor T0070907, showing an impaired activation of this receptor in adipose cells surrounding the breast cancer microenvironment. In conclusion, our study shows an impaired adipogenic differentiation capability in BC ADSCs. This suggests that the tumour microenvironment plays a key role in the modulation of the adipose microenvironment located in the surrounding tissue.

Project description:Unlabelled: Because adipose-derived stem cells (ASCs) are usually expanded to acquire large numbers of cells for therapeutic applications, it is important to increase the production yield and regenerative potential during expansion. Therefore, a tremendous need exists for alternative ASC stimuli during cultivation to increase the proliferation and adipogenic differentiation of ASCs. The present study primarily investigated the involvement of megestrol acetate (MA), a progesterone analog, in the stimulation of ASCs, and identifies the target receptors underlying stimulation. Mitogenic and adipogenic effects of MA were investigated in vitro, and pharmacological inhibition and small interfering (si) RNA techniques were used to identify the molecular mechanisms involved in the MA-induced stimulation of ASCs. MA significantly increased the proliferation, migration, and adipogenic differentiation of ASCs in a dose-dependent manner. Glucocorticoid receptor (GR) is highly expressed compared with other nuclear receptors in ASCs, and this receptor is phosphorylated after MA treatment. MA also upregulated genes downstream of GR in ASCs, including ANGPTL4, DUSP1, ERRF11, FKBP5, GLUL, and TSC22D3. RU486, a pharmacological inhibitor of GR, and transfection of siGR significantly attenuated MA-induced proliferation, migration, and adipogenic differentiation of ASCs. Although the adipogenic differentiation potential of MA was inferior to that of dexamethasone, MA had mitogenic effects in ASCs. Collectively, these results indicate that MA increases the proliferation, migration, and adipogenic differentiation of ASCs via GR phosphorylation.SignificanceMagestrol acetate (MA) increases the proliferation, migration, and adipogenic differentiation of adipose-derived stem cells (ASCs) via glucocorticoid receptor phosphorylation. Therefore, MA can be applied to increase the production yield during expansion and can be used to facilitate adipogenic differentiation of ASCs.

Dataset Information

FATP1 Exerts Variable Effects on Adipogenic Differentiation and Proliferation in Cells Derived From Muscle and Adipose Tissue.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets