%0 Journal Article
%T Regulation of bFGF-induced effects on rat aortic smooth muscle cells by β3-adrenergic receptors.
%A Chang Y
%A Dagat LA
%A Yusuf A
%A Zahriya Y
%A Staputyte K
%A Worley E
%A Holt A
%A Canuteson N
%A Messieha V
%A Halila K
%A Chang Y
%A Dagat LA
%A Yusuf A
%A Zahriya Y
%A Staputyte K
%A Worley E
%A Holt A
%A Canuteson N
%A Messieha V
%A Halila K
%J Curr Res Pharmacol Drug Discov
%V 3
%N 0
%D 2022
%M 35300074
暂无%R 10.1016/j.crphar.2022.100094
%X <B>UNASSIGNED: </B>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 β3-adrenergic receptors (β3-ARs) in vascular injury-induced neointima formation has not yet been defined.<BR><B>UNASSIGNED: </B>Our current study explored the possible role of β3-ARs in vascular injury-induced neointima formation by testing its effects on bFGF-induced VSMC migration and proliferation.<BR><B>UNASSIGNED: </B>β3-AR expression in rat carotid arteries was examined at 14 days following a balloon catheter-induced injury. The effects of β3-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.<BR><B>UNASSIGNED: </B>We found that vascular injury induced upregulation of β3-ARs in neointima. Pretreatment of VSMCs with a selective β3-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.<BR><B>UNASSIGNED: </B>Our results suggest that activation of β3-ARs potentiates bFGF-mediated effects on VSMCs by enhancing bFGF-mediated ERK and AKT phosphorylation and that β3-ARs may play a role in vascular injury-induced neointima formation.