Fig. 7: The schematic model for action mechanism of cP1P-induced therapeutic potential of UCB-MSCs. | Cell Death & Disease

Fig. 7: The schematic model for action mechanism of cP1P-induced therapeutic potential of UCB-MSCs.

From: O-cyclic phytosphingosine-1-phosphate stimulates HIF1α-dependent glycolytic reprogramming to enhance the therapeutic potential of mesenchymal stem cells

Fig. 7

cP1P stimulates intracellular calcium release through S1PR1 activation, which leads to PKCα/Akt/mTORC1 pathway activation. Activated mTORC1 increases HIF1α and BICD1 expression in a translation-dependent manner. BICD1 mediates upregulated HIF1α nuclear translocation, which is critical for HIF1 activation. HIF1 transcriptionally stimulates glycolysis-associated enzymes mRNA expression leading to glycolytic switch, which is critical for resistance to oxidative stress and apoptosis under hypoxia. Conclusively, cP1P-stimulated glycolysis enhances therapeutic potential of UCB-MSCs through HIF1α activation

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