Modulation of Adipogenic Conditions for Prospective Use of hADSCs in Adipose Tissue Engineering

被引:30
|
作者
Galateanu, Bianca [1 ]
Dinescu, Sorina [1 ]
Cimpean, Anisoara [1 ]
Dinischiotu, Anca [1 ]
Costache, Marieta [1 ]
机构
[1] Univ Bucharest, Dept Biochem & Mol Biol, Bucharest 050095, Romania
关键词
lipoaspirate; hADSC; adipogenesis; PPAR gamma 2; perilipin; aP2; FAS; Oil Red O; MESENCHYMAL STROMAL CELLS; PERFRINGENS ALPHA TOXIN; ISOLATED FAT CELLS; STEM-CELLS; PPAR-GAMMA; ENDOTHELIAL-CELLS; BINDING PROTEIN; IN-VITRO; DIFFERENTIATION; METABOLISM;
D O I
10.3390/ijms131215881
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Modern strategies in adipose tissue engineering (ATE) take advantage of the easy harvest, abundance and differentiation potential towards mesenchymal lineages of hADSCs. The controlled conversion of hADSCs to committed adipogenic precursors and further mature adipocytes formation is important for good long-term results in soft tissue regeneration. Thus, in this study, we report: (i) the isolation of the processed lipoaspirate (PLA) cells from adipose tissue and sanguine fractions; (ii) the phenotypic characterization of the PLA descendants; (iii) the design of a novel protocol for the modulation of adipogenic conditions in the perspectives of ATE applications. To modulate the differentiation rate through our protocol, we propose to selectively modify the formulation of the adipogenic media in accordance with the evolution of the process. Therefore, we aimed to ensure the long-term proliferation of the precursor cells and to delay the late adipogenic events. The status of differentiation was characterized in terms of intracellular lipid accumulation and reorganization of the cytoskeleton simultaneously with perilipin protein expression. Moreover, we studied the sequential activation of PPAR gamma 2, FAS, aP2 and perilipin genes which influence the kinetics of the adipogenic process. The strategies developed in this work are the prerequisites for prospective 3D regenerative systems.
引用
收藏
页码:15881 / 15900
页数:20
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