Regulation of bFGF-induced effects on rat aortic smooth muscle cells by β 3 -adrenergic receptors

• Published in: Current research in pharmacology and drug discovery 2022, Vol.3, p.100094
• Main Authors: Chang, Yingzi, Dagat, Lei Alena, Yusuf, Aisha, Zahriya, Yusuf, Staputyte, Kotryna, Worley, Emma, Holt, Alex, Canuteson, Natalie, Messieha, Vereena, Halila, Kasey
• Format: Article
• Language: English
• ISSN: 2590-2571

Basic fibroblast growth factor (bFGF)-mediated vascular smooth muscle cell (VSMC) proliferation and migration play an important role in vascular injury-induced neointima formation and subsequent vascular restenosis, a major event that hinders the long-term success of angioplasty. The function of β -adrenergic receptors (β -ARs) in vascular injury-induced neointima formation has not yet been defined. Our current study explored the possible role of β -ARs in vascular injury-induced neointima formation by testing its effects on bFGF-induced VSMC migration and proliferation. β -AR expression in rat carotid arteries was examined at 14 days following a balloon catheter-induced injury. The effects of β -AR activation on bFGF-induced rat aortic smooth muscle cell proliferation, migration, and signaling transduction (including extracellular-signal-regulated kinase/mitogen activated protein kinase, ERK/MAPK and Protein kinase B, AKT) were tested. We found that vascular injury induced upregulation of β -ARs in neointima. Pretreatment of VSMCs with a selective β -AR agonist, CL316,243 significantly potentiated bFGF-induced cell migration and proliferation, and ERK and AKT phosphorylation. Our results also revealed that suppressing phosphorylation of ERK and AKT blocked bFGF-induced cell migration and that inhibiting AKT phosphorylation reduced bFGF-mediated cell proliferation. Our results suggest that activation of β -ARs potentiates bFGF-mediated effects on VSMCs by enhancing bFGF-mediated ERK and AKT phosphorylation and that β -ARs may play a role in vascular injury-induced neointima formation.