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Journal of Experimental Hematology ; (6): 569-575, 2018.
Article in Chinese | WPRIM | ID: wpr-690948

ABSTRACT

<p><b>OBJECTIVE</b>To study the effect and mechanism of mTOR signaling on adipogenesis of bone marrow mesenchymal stem cells(BM-MSCs) from aplastic anemia (AA) patients through regulation of PPARγ.</p><p><b>METHODS</b>BM-MSCs were isolated from 24 newly diagnosed AA patients and 24 healthy controls. The surface antigen expression of BM-MSCs was identified by flow cytometry. The capacity of adipogenic differentiation of BM-MSCs was determined by lipid droplets based on Oil Red O staining and by the expression of FABP4 based on Western blot. Protein levels of mTOR signaling and PPARγ were tested by immunofluorescence and Western blot.</p><p><b>RESULTS</b>AA BM-MSCs displayed an enhanced capacity of differentiating into adipocytes, compared with control BM-MSCs. It was found that mTOR was activated in AA BM-MSCs. Moreover, the expression levels of p-mTOR and PPAR-γ in AA BM-MSCs showed a parallel differentiation-dependent increase during adipogenic differentiation, which were significantly higher than that of control BM-MSCs at the same time point of adipogenic differentiation. mTOR inhibitor rapamycin did not only inhibit the adipogenic differentiation of BM-MSCs from AA pateints at the early-middle stage, but also partly reversed the adipogenic differention of BM-MSCs from AA pateints at the late stage by PPARγ regulation.</p><p><b>CONCLUSION</b>mTOR signaling may play a critical role in the adipogenic differentiation of BM-MSCs from AA patients by positively regulating PPARγ expression.</p>


Subject(s)
Humans , Adipogenesis , Anemia, Aplastic , Bone Marrow Cells , Cell Differentiation , Cells, Cultured , Mesenchymal Stem Cells , PPAR gamma , Signal Transduction , TOR Serine-Threonine Kinases
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