Active caspase9 procaspase3 Active caspase3 cleaved substrates substrates cytochrome c Apaf1 ATP cytochrome c Apoptosome Apoptosis BMSCs BMSCs BMSCs BMSCs Bcl2 Bax ID: 1041854
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1. compressionprocaspase-9Active caspase-9procaspase-3Active caspase-3cleaved substratessubstratescytochrome c Apaf-1 ATPcytochrome cApoptosomeApoptosisBMSCsBMSCsBMSCsBMSCsBcl-2Bax: paracrine factorscytoplasmROSROSNPCs : mechanosensors(Need further study)
2. Figure.S1: The schematic diagram of the mechanism and signaling pathway of the antiapoptosis effect of BMSCs on NPCs under compression. Compression loadings enhanced the production of ROS, decreased mitochondrial membrane potential, suppressed the expression of Bcl-2 and increased the expression of Bax. And the Bax/Bcl-2 complex dissociation led to the release of cytochrome c. Cytochrome c, along with Apaf-1 and caspase-9, formed multiprotein apoptosome, which ultimately produced cleaved caspase-9, 3 and led to the cell apoptosis. These effects were significantly attenuated by coculturing with BMSCs. The potential mechanosensors of NPCs and paracrine factors secreted by BMSCs remain to be explored.