Figure 7.

Schematic Representation of PDGFR, ERK, and SMAD Signaling in AdMSCs

In AdMSCs from healthy donors, PDGF binding to its receptor activates ERK signaling, which in turn induces the translocation of SMAD to the nucleus and its phosphorylation. The activation of ERK and SMAD promotes the transcription of their target genes, including Tf. In AdMSCs derived from diabetic patients, PDGF signaling is downregulated, which results in partial inhibition of ERK1/2. However, SMAD is upregulated in AdMSCs derived from diabetic patients; consequently, TF expression is enhanced. This suggests that other pathways are involved in the sustained activation of SMAD observed in AdMSCs derived from diabetic patients.