Translocation of protein kinase C-δ by PDGF in cultured vascular smooth muscle cells: Inhibition by TGF-β1
platelet-derived growth factor; protein kinase C; transforming growth factor-β1; vascular smooth muscle
The migration and proliferation of vascular smooth muscle cells (SMC) into the neointima are important early events in the development of atherosclerosis and post-angioplasty restenosis. The stimulation of SMC migration by platelet derived growth factor (PDGF) involves the induction of protein kinase C activity. Using immunoblot techniques, we demonstrated that rat aortic SMC express a pattern of PKC isoforms which includes PKC-α, δ, ε, ζ, and η. Upon exposure to PDGF-BB, a fraction of PKC-δ was rapidly translocated from the cytosol to the post-nuclear particulate fraction at 15 seconds and reached an apparent maximum at 30 minutes. In contrast, PKC-α and ζ were not translocated by PDGF-BB. TGF-β1, which inhibits PDGF- induced DNA synthesis and chemotaxis, reduced the immunoreactive levels of PKC-δ and blocked the PDGF-induced translocation of PKC-δ to the particulate fraction. This suggests that the activation of PKC-δ by translocation to the particulate fraction may play an important role in the control of vascular smooth muscle cell migration by PDGF and TGF-β1.
Leng, L., Du, B., Consigli, S., & McCaffrey, T. (1996). Translocation of protein kinase C-δ by PDGF in cultured vascular smooth muscle cells: Inhibition by TGF-β1. Artery, 22 (3). Retrieved from https://hsrc.himmelfarb.gwu.edu/smhs_medicine_facpubs/4878