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dc.creatorShan, Dan
dc.creatorQu, Ping
dc.creatorZhong, Chao
dc.creatorHe, Luling
dc.creatorZhang, Qingshan
dc.creatorZhong, Guoyue
dc.creatorHu, Wenhui
dc.creatorFeng, Yulin
dc.creatorYang, Shilin
dc.creatorYang, Xiaofeng
dc.creatorYu, Jun
dc.identifier.citationShan D, Qu P, Zhong C, He L, Zhang Q, Zhong G, Hu W, Feng Y, Yang S, Yang X-f and Yu J (2022) Anemoside B4 Inhibits Vascular Smooth Muscle Cell Proliferation, Migration, and Neointimal Hyperplasia. Front. Cardiovasc. Med. 9:907490. doi: 10.3389/fcvm.2022.907490
dc.description.abstractVascular smooth muscle cell (VSMC) phenotypic transformation, proliferation, and migration play a pivotal role in developing neointimal hyperplasia after vascular injury, including percutaneous transluminal angioplasty and other cardiovascular interventions. Anemoside B4 (B4) is a unique saponin identified from the Pulsatilla chinensis (Bge.) Regel, which has known anti-inflammatory activities. However, its role in modulating VSMC functions and neointima formation has not been evaluated. Herein, we demonstrate that B4 administration had a potent therapeutic effect in reducing neointima formation in a preclinical mouse femoral artery endothelium denudation model. Bromodeoxyuridine incorporation study showed that B4 attenuated neointimal VSMC proliferation in vivo. Consistent with the in vivo findings, B4 attenuated PDGF-BB-induced mouse VSMC proliferation and migration in vitro. Moreover, quantitative RT-PCR and Western blot analysis demonstrated that B4 suppressed PDGF-BB-induced reduction of SM22α, SMA, and Calponin, suggesting that B4 inhibited the transformation of VSMCs from contractile to the synthetic phenotype. Mechanistically, our data showed B4 dose-dependently inhibited the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT and p38 mitogen-activated protein kinase MAPK signaling pathways. Subsequently, we determined that B4 attenuated VSMC proliferation and migration in a p38 MAPK and AKT dependent manner using pharmacological inhibitors. Taken together, this study identified, for the first time, Anemoside B4 as a potential therapeutic agent in regulating VSMC plasticity and combating restenosis after the vascular intervention.
dc.format.extent12 pages
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartFrontiers in Cardiovascular Medicine, Vol. 9
dc.relation.isreferencedbyFrontiers Media
dc.rightsAttribution CC BY
dc.subjectAnemoside B4
dc.subjectVascular smooth muscle cell
dc.subjectNeointimal hyperplasia
dc.titleAnemoside B4 Inhibits Vascular Smooth Muscle Cell Proliferation, Migration, and Neointimal Hyperplasia
dc.type.genreJournal article
dc.contributor.groupCenter for Metabolic Disease Research (Temple University)
dc.description.departmentCardiovascular Sciences
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact
dc.description.schoolcollegeLewis Katz School of Medicine
dc.temple.creatorShan, Dan
dc.temple.creatorQu, Ping
dc.temple.creatorZhong, Chao
dc.temple.creatorHu, Wenhui
dc.temple.creatorYang, Xiao-Feng
dc.temple.creatorYu, Jun

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