Rosuvastatin suppresses platelet‑derived growth factor‑BB‑induced vascular smooth muscle cell proliferation and migration via the MAPK signaling pathway Retraction in /10.3892/etm.2023.12299

Gan,Jianting; Li,Ping; Wang,Zhengdong; Chen,Jian; Liang,Xiangwen; Liu,Ming; Xie,Wenchao; Yin,Ruixing; Huang,Feng

doi:10.3892/etm.2013.1265

October 2013 Volume 6 Issue 4

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October 2013 Volume 6 Issue 4

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Article

Rosuvastatin suppresses platelet‑derived growth factor‑BB‑induced vascular smooth muscle cell proliferation and migration via the MAPK signaling pathway

Retraction in: /10.3892/etm.2023.12299

Authors:
- Jianting Gan
- Ping Li
- Zhengdong Wang
- Jian Chen
- Xiangwen Liang
- Ming Liu
- Wenchao Xie
- Ruixing Yin
- Feng Huang
View Affiliations / Copyright

Affiliations: Department of Cardiology, Sixth Affiliated Hospital of Guangxi Medical University, Yulin, Guangxi 537000, P.R. China, Department of Cardiology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
Pages: 899-903
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Published online on: August 20, 2013

https://doi.org/10.3892/etm.2013.1265
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Abstract

An imbalance in the proliferation and migration of vascular smooth muscle cells (VSMCs) is significant in the onset and progression of vascular diseases, including arteriosclerosis and restenosis subsequent to vein grafting or coronary intervention. Rosuvastatin, a selective inhibitor of hydroxymethylglutaryl coenzyme A (HMG‑CoA) reductase, has pharmacological properties including the ability to reduce low‑density lipoprotein‑cholesterol (LDL‑C) and very low‑density lipoprotein‑cholesterol (VLDL‑C) levels, slow atherosclerosis progression and improve coronary heart disease outcomes. However, little is known concerning the molecular mechanism by which rosuvastatin affects vascular cell dynamics. In this study, we studied the inhibitory role of rosuvastatin on platelet‑derived growth factor‑BB (PDGF‑BB)‑induced VSMC proliferation and migration, as well as the molecular mechanisms involved. MTT data showed that rosuvastatin markedly inhibited the proliferation of PDGF‑BB‑induced VSMCs in a time‑dependent manner. VSMCs are able to dedifferentiate into a proliferative phenotype in response to PDGF‑BB stimulation; however, rosuvastatin effectively attenuated this phenotype switching. Moreover, we also showed that rosuvastatin significantly suppressed PDGF‑BB‑induced VSMC migration, which may be a result of its inhibitory effect on the protein expression of matrix metalloproteinase‑2 (MMP2) and MMP9. Investigation into the molecular mechanisms involved revealed that rosuvastatin inhibited the mitogen‑activated protein kinase (MAPK) signaling pathway by downregulating extracellular signal‑regulated kinase (ERK) and p38 MAPK, although the phosphorylation level of c‑Jun N‑terminal kinase (c‑JNK) was not altered following rosuvastatin treatment. In conclusion, the present study showed that rosuvastatin suppressed PDGF‑BB‑induced VSMC proliferation and migration, indicating that rosuvastatin has the potential to become a promising therapeutic agent for the treatment of atherosclerosis and restenosis.

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