Platonin inhibited PDGF-BB-induced proliferation of rat vascular smooth muscle cells via JNK1/2-dependent signaling

Yi Chang, Yih Huei Uen, Chang Chih Chen, Song-Chow Lin, Shiao Yun Tseng, Yi Hsuan Wang, Joen Rong Sheu, Cheng Ying Hsieh

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Aim:To examine the inhibitory actions of the immunoregulator platonin against proliferation of rat vascular smooth muscle cells (VSMCs).Methods:VSMCs were prepared from the thoracic aortas of male Wistar rats. Cell proliferation was examined using MTT assays. Cell cycles were analyzed using flow cytometry. c-Jun N-terminal kinase (JNK)1/2, extracellular signal-regulated kinase (ERK)1/2, AKT, and c-Jun phosphorylation or p27 expression were detected using immunoblotting.Results:Pretreatment with platonin (1-5 μmol/L) significantly suppressed VSMC proliferation stimulated by PDGF-BB (10 ng/mL) or 10% fetal bovine serum (FBS), and arrested cell cycle progression in the S and G 2/M phases. The same concentrations of platonin significantly inhibited the phosphorylation of JNK1/2 but not ERK1/2 or AKT in VSMCs stimulated by PDGF-BB. Furthermore, platonin also attenuated c-Jun phosphorylation and markedly reversed the down-regulation of p27 expression after PDGF-BB stimulation.Conclusion:Platonin inhibited VSMC proliferation, possibly via inhibiting phosphorylation of JNK1/2 and c-Jun, and reversal of p27 down-regulation, thereby leading to cell cycle arrest at the S and G 2/M phases. Thus, platonin may represent a novel approach for lowering the risk of abnormal VSMC proliferation and related vascular diseases.

Original languageEnglish
Pages (from-to)1337-1344
Number of pages8
JournalActa Pharmacologica Sinica
Volume32
Issue number11
DOIs
Publication statusPublished - Nov 2011

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Vascular Smooth Muscle
Smooth Muscle Myocytes
Phosphorylation
Cell Proliferation
Cell Division
Cell Cycle
Down-Regulation
Mitogen-Activated Protein Kinase 9
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase 1
Cell Cycle Checkpoints
Thoracic Aorta
Vascular Diseases
Immunoblotting
platelet-derived growth factor BB
platonin
Wistar Rats
Flow Cytometry
Serum

Keywords

  • cell cycle
  • JNK1/2
  • p27
  • PDGF-BB
  • vascular smooth muscle cells

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Platonin inhibited PDGF-BB-induced proliferation of rat vascular smooth muscle cells via JNK1/2-dependent signaling. / Chang, Yi; Uen, Yih Huei; Chen, Chang Chih; Lin, Song-Chow; Tseng, Shiao Yun; Wang, Yi Hsuan; Sheu, Joen Rong; Hsieh, Cheng Ying.

In: Acta Pharmacologica Sinica, Vol. 32, No. 11, 11.2011, p. 1337-1344.

Research output: Contribution to journalArticle

Chang, Yi ; Uen, Yih Huei ; Chen, Chang Chih ; Lin, Song-Chow ; Tseng, Shiao Yun ; Wang, Yi Hsuan ; Sheu, Joen Rong ; Hsieh, Cheng Ying. / Platonin inhibited PDGF-BB-induced proliferation of rat vascular smooth muscle cells via JNK1/2-dependent signaling. In: Acta Pharmacologica Sinica. 2011 ; Vol. 32, No. 11. pp. 1337-1344.
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AU - Chen, Chang Chih

AU - Lin, Song-Chow

AU - Tseng, Shiao Yun

AU - Wang, Yi Hsuan

AU - Sheu, Joen Rong

AU - Hsieh, Cheng Ying

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N2 - Aim:To examine the inhibitory actions of the immunoregulator platonin against proliferation of rat vascular smooth muscle cells (VSMCs).Methods:VSMCs were prepared from the thoracic aortas of male Wistar rats. Cell proliferation was examined using MTT assays. Cell cycles were analyzed using flow cytometry. c-Jun N-terminal kinase (JNK)1/2, extracellular signal-regulated kinase (ERK)1/2, AKT, and c-Jun phosphorylation or p27 expression were detected using immunoblotting.Results:Pretreatment with platonin (1-5 μmol/L) significantly suppressed VSMC proliferation stimulated by PDGF-BB (10 ng/mL) or 10% fetal bovine serum (FBS), and arrested cell cycle progression in the S and G 2/M phases. The same concentrations of platonin significantly inhibited the phosphorylation of JNK1/2 but not ERK1/2 or AKT in VSMCs stimulated by PDGF-BB. Furthermore, platonin also attenuated c-Jun phosphorylation and markedly reversed the down-regulation of p27 expression after PDGF-BB stimulation.Conclusion:Platonin inhibited VSMC proliferation, possibly via inhibiting phosphorylation of JNK1/2 and c-Jun, and reversal of p27 down-regulation, thereby leading to cell cycle arrest at the S and G 2/M phases. Thus, platonin may represent a novel approach for lowering the risk of abnormal VSMC proliferation and related vascular diseases.

AB - Aim:To examine the inhibitory actions of the immunoregulator platonin against proliferation of rat vascular smooth muscle cells (VSMCs).Methods:VSMCs were prepared from the thoracic aortas of male Wistar rats. Cell proliferation was examined using MTT assays. Cell cycles were analyzed using flow cytometry. c-Jun N-terminal kinase (JNK)1/2, extracellular signal-regulated kinase (ERK)1/2, AKT, and c-Jun phosphorylation or p27 expression were detected using immunoblotting.Results:Pretreatment with platonin (1-5 μmol/L) significantly suppressed VSMC proliferation stimulated by PDGF-BB (10 ng/mL) or 10% fetal bovine serum (FBS), and arrested cell cycle progression in the S and G 2/M phases. The same concentrations of platonin significantly inhibited the phosphorylation of JNK1/2 but not ERK1/2 or AKT in VSMCs stimulated by PDGF-BB. Furthermore, platonin also attenuated c-Jun phosphorylation and markedly reversed the down-regulation of p27 expression after PDGF-BB stimulation.Conclusion:Platonin inhibited VSMC proliferation, possibly via inhibiting phosphorylation of JNK1/2 and c-Jun, and reversal of p27 down-regulation, thereby leading to cell cycle arrest at the S and G 2/M phases. Thus, platonin may represent a novel approach for lowering the risk of abnormal VSMC proliferation and related vascular diseases.

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