UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED:我们目前的研究通过测试β3-ARs对bFGF诱导的VSMC迁移和增殖的影响,探索了β3-ARs在血管损伤诱导的新内膜形成中的可能作用。
未经证实:在球囊导管诱导的损伤后14天检查了大鼠颈动脉中β3-AR的表达。β3-AR激活对bFGF诱导的大鼠主动脉平滑肌细胞增殖的影响,迁移,和信号转导(包括细胞外信号调节激酶/丝裂原活化蛋白激酶,ERK/MAPK与蛋白激酶B,AKT)进行了测试。
未经证实:我们发现血管损伤引起新内膜中β3-ARs的上调。用选择性β3-AR激动剂预处理VSMC,CL316,243显着增强bFGF诱导的细胞迁移和增殖,ERK和AKT磷酸化。我们的结果还表明,抑制ERK和AKT的磷酸化可阻断bFGF诱导的细胞迁移,而抑制AKT磷酸化可降低bFGF介导的细胞增殖。
UNASSIGNED:我们的结果表明,β3-ARs的激活通过增强bFGF介导的ERK和AKT磷酸化来增强bFGF介导的VSMCs的作用,并且β3-ARs可能在血管损伤诱导的新内膜形成中起作用。