Figure 8

PDGF-BB employs PDGFR-β in hemSCs. shRNA-mediated knockdown of PDGFR-α (a) and PDGFR-β (b) in hemSCs at sub-passage 1 (subP1; following 2 weeks of puromycin selection) and sub-passage 6 (six serial passages after puromycin selection) (*P<0.05 compared with control shRNA). (c) shRNA-knockdown of PDGFR-α and PDGFR-β in hemSCs reduced the inhibitory effect of PDGF-BB on hemSC adipogenesis (*P<0.05 compared with control shRNA). (d) Schematic illustrating the findings of the study and our working hypothesis. High levels of PDGF-BB from hemSCs during proliferation mediate intracellular signaling through PDGFR-β (predominantly PDGFR-ββ homodimer with contribution from PDGFR-αβ heterodimer) to inhibit C/EBPα and PPARγ expression and adipogenesis (i.e., involution). Upon regression of the vessels and removal of the PDGF-BB source, adipogenesis is triggered