Iptakalim inhibits PDGF-BB-induced human airway smooth muscle cells proliferation and migration.

摘要: Abstract Chronic airway diseases are characterized by remodeling which is attributed partly to the proliferation and migration of smooth muscle cells (ASMCs). ATP-sensitive potassium (K ATP ) channels have been identified in ASMCs. Mount evidence has suggested that K channel openers can reduce hyperresponsiveness alleviate remodeling. Opening + triggers efflux, leading membrane hyperpolarization, preventing Ca 2+ entry through closing voltage-operated channels. Intracellular most important regulator contraction, cell migration. efflux decreases influx, consequently influences ASMCs As a opener, iptakalim (Ipt) reported restrain pulmonary arterial (PASMCs) involved vascular remodeling, while little known about its impact on The present study was designed investigate effects Ipt human mechanisms underlying. Results obtained from counting kit-8 (CCK-8), flow cytometry 5-ethynyl-2′-deoxyuridine (EdU) incorporation showed significantly inhibited platelet-derived growth factor (PDGF)-BB-induced proliferation. induced PDGF-BB also suppressed transwell scratch assay. Besides, phosphorylation /calmodulin-dependent kinase II (CaMKII), extracellular regulated protein kinases 1/2 (ERK1/2), B (Akt), cyclic adenosine monophosphate (cAMP) response element binding (CREB) were as well alleviated administration. Furthermore, we found inhibition PDGF-BB-induced blocked glibenclamide (Gli), selective antagonist. These findings provide strong support antagonize proliferating migrating opening Altogether, our results highlighted novel profile potent option against chronic diseases.