| First Author | Kato Y | Year | 2019 |
| Journal | J Physiol Sci | Volume | 69 |
| Issue | 2 | Pages | 175-184 |
| PubMed ID | 30084082 | Mgi Jnum | J:311948 |
| Mgi Id | MGI:6781569 | Doi | 10.1007/s12576-018-0631-7 |
| Citation | Kato Y, et al. (2019) Epac1 deficiency inhibits basic fibroblast growth factor-mediated vascular smooth muscle cell migration. J Physiol Sci 69(2):175-184 |
| abstractText | Vascular smooth muscle cell (VSMC) migration and the subsequent intimal thickening play roles in vascular restenosis. We previously reported that an exchange protein activated by cAMP 1 (Epac1) promotes platelet-derived growth factor (PDGF)-induced VSMC migration and intimal thickening. Because basic fibroblast growth factor (bFGF) also plays a pivotal role in restenosis, we examined whether Epac1 was involved in bFGF-mediated VSMC migration. bFGF-induced lamellipodia formation and migration were significantly decreased in VSMCs obtained from Epac1(-/-) mice compared to those in Epac1(+/+)-VSMCs. The bFGF-induced phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta), which play a role in bFGF-induced cell migration, was attenuated in Epac1(-/-)-VSMCs. Intimal thickening induced by the insertion of a large wire was attenuated in Epac1(-/-) mice, and was accompanied by the decreased phosphorylation of GSK3beta. These data suggest that Epac1 deficiency attenuates bFGF-induced VSMC migration, possibly via Akt/GSK3beta pathways. |
