Loading...
Anemoside B4 Inhibits Vascular Smooth Muscle Cell Proliferation, Migration, and Neointimal Hyperplasia
Shan, Dan Qu, Ping Zhong, Chao He, Luling Zhang, Qingshan Zhong, Guoyue Feng, Yulin Yang, Shilin
Shan, Dan
Qu, Ping
Zhong, Chao
He, Luling
Zhang, Qingshan
Zhong, Guoyue
Feng, Yulin
Yang, Shilin
Citations
Altmetric:
Genre
Journal article
Date
2022-05-10
Advisor
Committee member
Department
Cardiovascular Sciences
Permanent link to this record
Collections
Research Projects
Organizational Units
Journal Issue
DOI
http://dx.doi.org/10.3389/fcvm.2022.907490
Abstract
Vascular 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.
Description
Citation
Shan 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
Citation to related work
Frontiers Media
Has part
Frontiers in Cardiovascular Medicine, Vol. 9
ADA compliance
For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu