GSE186026
Transcriptomic analyses of the anti-adipogenic and pro-osteoblastic effects of aspirin in rat bone mesenchymal stem cell
Theoretically, the differentiation of mesenchymal stem cells (MSCs) into either adipocytic or osteoblastic phenotype can be deemed as a seesaw, where induction of one lineage comes at the expense of the other. Previously, researchers, including our team, found that aspirin promoted osteoblast differentiation of bone mesenchymal stem cells (BMSCs) whereas inhibiting adipogenic differentiation. However, the precise mechanisms, that is, which pathways, what biological process or key genes involved during this process, had not been systematically studied. In the present study, we tend to analyze the whole transcriptome of the anti-adipogenic and promote-osteoblastic effects of aspirin in BMSCs. Our results showed that aspirin's presence restored or further strengthened the expression of an important part of the gene population repressed during adipogenesis or increased during osteogenesis. Besides, classical pathways related to osteogenic differentiation (p53 signaling pathway, focal adhesion, osteoclast differentiation, PI3K-Akt signaling pathway, MAPK signaling pathway, and Wnt signaling pathway) and the fat metabolism were also disturbed during the promote-osteoblastic and anti-adipogenic effects of aspirin. Therefore, our whole-genome transcriptomic results shed new light and open the door to more specific “omics” studies. Our results allow a better understanding of the anti-adipogenic and promote-osteoblastic effects of aspirin and pave the way to aspirin clinical use for the prevention and treatment of diseases like tissue defect and osteoporosis. Overall design: The whole-genome transcriptome of the anti-adipogenic and promote-osteoblastic effects of aspirin in rat bone mesenchymal stem cells