fig2

Figure 2. Schematic representation of EV-mediated TGF-β and EGF signaling. A: TGF-β is inactive because of its interaction with LAP. When it dissociates from LAP upon mechanical interaction between LAP and integrins on the membrane, EVs containing TGF-β influence biological processes by binding to TGF-β receptors on the cell surface, whose kinase substrates are the transcription factors of the Smad family. EVs may carry TGF-β type II receptors that are transferred to cells devoid of them, resulting in the activation of TGF-β signaling; B: EGF receptor family members are present on the EV surface. They can be transferred via EVs to cells lacking them, leading to the activation of downstream signaling pathways. EVs may also contain EGFR ligands, leading to the activation of downstream signaling pathways in cells already expressing EGFRs. EV: Extracellular vesicles; TGF-β: transforming growth factor β; EGF: epidermal growth factor; LAP: latency-associated peptide; EGFR: EGF receptor.