PDF(Pubmed)
Abstract：
UNASSIGNED: 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.
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: 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.
摘要：
未经证实：碱性成纤维细胞生长因子（bFGF）介导的血管平滑肌细胞（VSMC）的增殖和迁移在血管损伤诱导的新内膜形成和随后的血管再狭窄中起重要作用，阻碍血管成形术长期成功的重大事件。β3-肾上腺素能受体（β3-ARs）在血管损伤诱导的新内膜形成中的功能尚未确定。
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。
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。
