Anti-proliferative actions of 2-decylamino-5,8-dimethoxy-1,4-naphthoquinone in vascular smooth muscle cells

Lee, Jung‐Jin; Zhang, Weiyun; Yi, Hyoseok; Kim, Young S.; Kim, In-Su; Shen, Gui‐Nan; Song, Gyu Yong; Myung, Chang‐Seon

doi:10.1016/j.bbrc.2011.06.145

Cited by 16 publications

(20 citation statements)

References 24 publications

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“…Degradation of the ECM promoted VSMC migration from the media of arterial walls to the intimal space, where VSMCs secreted more ECM products, progressively resulting in restenosis and neointima formation [40, 41]. Moreover, several migration regulatory proteins, including cell adhesion molecules ICAM-1, VCAM-1 [27, 42], MMP2, and MMP-9 were reported to be vital regulators of abnormal VSMC migration [43-45]. In the present study, our results indicated that atorvastatin calcium inhibited the expression of ICAM-1, VCAM-1, MMP2, and MMP-9 induced by PDGF-ββ stimulation.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin Calcium Inhibits PDGF-ββ-Induced Proliferation and Migration of VSMCs Through the G0/G1 Cell Cycle Arrest and Suppression of Activated PDGFRβ-PI3K-Akt Signaling Cascade

Chen¹,

Dong²,

Zhao³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Abnormal proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of vascular lesions, such as atherosclerosis and restenosis. PDGF-ββ, an isoform of PDGF (platelet-derived growth factor), has been demonstrated to induce proliferation and migration of VSMCs. Atorvastatin calcium, a selective inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, has favorable protective effects on VSMCs. This study examined the effects of atorvastatin calcium on the proliferation and migration of PDGF-ββ-treated VSMCs, as well as its underlying mechanisms. Methods: MTT assays, Edu imaging, cell cycle analysis, wound healing assays, transwell migration assays, and western blot analysis were performed. Results: Atorvastatin calcium significantly inhibited cell proliferation, DNA synthesis and cell migration of PDGF-ββ-treated VSMCs. We demonstrated that atorvastatin calcium induced cell cycle arrest in the G0/G1 phase in response to PDGF-ββ stimulation and decreased the expression of G0/G1-specific regulatory proteins, including proliferating cell nuclear antigen (PCNA), CDK2, cyclin D1, cyclin E and CDK4 in PDGF-ββ-treated VSMCs. Moreover, pretreatment with atorvastatin calcium inhibited the PDGF-ββ-treated phosphorylation of PDGFRβ and Akt, whereas atorvastatin calcium did not affect the phosphorylation of PLC-γ1 or (ERK) 1/2. Conclusion: Our data suggested that atorvastatin calcium inhibited abnormal proliferation and migration of VSMCs through G0/G1 cell cycle arrest and suppression of the PDGFRβ-Akt signaling cascade.

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Section: Discussionmentioning

confidence: 99%

Atorvastatin Calcium Inhibits PDGF-ββ-Induced Proliferation and Migration of VSMCs Through the G0/G1 Cell Cycle Arrest and Suppression of Activated PDGFRβ-PI3K-Akt Signaling Cascade

Chen¹,

Dong²,

Zhao³

et al. 2017

Cell Physiol Biochem

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“…Our previous study demonstrated that early signal, such as Akt, ERK1/2 and PLCγ1 phosphorylation, is important signal transduction in hyper-proliferation of VSMCs [26,29]. Hence, to investigate the role of early signalling events in the antiproliferative activity of S-A144, phosphorylation of Akt, ERK1/2 and PLCγ1 was measured in VSMCs following stimulation with PDGF-BB.…”

Section: Resultsmentioning

confidence: 99%

Fermented soshiho-tang with Lactobacillus plantarum enhances the antiproliferative activity in vascular smooth muscle cell

Lee

Kwon

Lee

et al. 2014

BMC Complement Altern Med

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BackgroundSoshiho-tang (SST) is a traditional medicine widely used for the treatment of chronic hepatitis. SST has been shown to confer a variety of pharmacological activities, including prevention of hepatotoxicity, promotion of liver regeneration, and modulation of liver fibrosis. In this study, we investigated the antiproliferative activity of native and fermented (FSST) formulations of SST in vascular smooth muscle cells (VSMCs) and examined the potential underlying mechanisms driving these effects.MethodsSST, along with preparations fermented with Lactobacillus plantarum KFRI-144 (S-A144), L. amylophilus KFRI-161 (S-A161) and L. bulgaricus KFRI-344 (S-A344), were investigated to determine their effects on the proliferation and viability of VSMCs, along with the signalling pathways underlying these effects.ResultsS-A144 exhibited a strong, dose-dependent inhibition of VSMC proliferation relative to untreated controls, but the others did not affect. In addition, S-A144 significantly decreased the phosphorylation of Akt and PLCγ1 in a dose-dependent manner and induced cell cycle arrest at the G0/G1 phase characterised by decreased expression of CDKs, cyclins and PCNA.ConclusionsThe findings suggest that S-A144 exhibit enhanced inhibition of PDGF-BB-induced VSMC proliferation comparison to S-AOR through the suppression of cell cycle progression and expression of cell cycle-related proteins, along with the downregulation of Akt phosphorylation.

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“…Cell culture conditions were as described previously [19,21,22]. The purity of VSMCs was confirmed by immunocytochemical localization of β-smooth-muscle actin.…”

Section: Methodsmentioning

confidence: 99%

“…Both direct cell counting and nonradioactive colorimetric WST-1 assay (premix WST-1, Takara, Japan) were used to measure VSMC proliferation, as described previously [19,21,22]. For direct cell counting, VSMCs were treated with various concentrations of 2-nonylamino-DMNQ for 24 h in serum-free medium and stimulated with PDGF-BB (25 ng/ml).…”

Section: Methodsmentioning

confidence: 99%

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5,8-Dimethoxy-2-Nonylamino-Naphthalene-1,4-Dione Inhibits Vascular Smooth Muscle Cell Proliferation by Blocking Autophosphorylation of PDGF-Receptor β

Kim

Lee

et al. 2013

Korean J Physiol Pharmacol

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As the abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a critical role in the development of atherosclerosis and vascular restenosis, a candidate drug with antiproliferative properties is needed. We investigated the antiproliferative action and underlying mechanism of a newly synthesized naphthoquinone derivative, 5,8-dimethoxy-2-nonylamino-naphthalene-1,4-dione (2-nonylamino-DMNQ), using VSMCs treated with platelet-derived growth factor (PDGF). 2-Nonylamino-DMNQ inhibited proliferation and cell number of VSMCs induced by PDGF, but not epidermal growth factor (EGF), in a concentration-dependent manner without any cytotoxicity. This derivative suppressed PDGF-induced [3H]-thymidine incorporation, cell cycle progression from G0/G1 to S phase, and the phosphorylation of phosphor-retinoblastoma protein (pRb) as well as the expression of cyclin E/D, cyclin-dependent kinase (CDK) 2/4, and proliferating cell nuclear antigen (PCNA). Importantly, 2-nonylamino-DMNQ inhibited the phosphorylation of PDGF receptorβ(PDGF-Rβ) enhanced by PDGF at Tyr579, Tyr716, Tyr751, and Tyr1021 residues. Subsequently, 2-nonylamino-DMNQ inhibited PDGF-induced phosphorylation of STAT3, ERK1/2, Akt, and PLCγ1. Therefore, our results indicate that 2-nonylamino-DMNQ inhibits PDGF-induced VSMC proliferation by blocking PDGF-Rβ autophosphorylation, and subsequently PDGF-Rβ-mediated downstream signaling pathways.

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Anti-proliferative actions of 2-decylamino-5,8-dimethoxy-1,4-naphthoquinone in vascular smooth muscle cells

Cited by 16 publications

References 24 publications

Atorvastatin Calcium Inhibits PDGF-ββ-Induced Proliferation and Migration of VSMCs Through the G0/G1 Cell Cycle Arrest and Suppression of Activated PDGFRβ-PI3K-Akt Signaling Cascade

Atorvastatin Calcium Inhibits PDGF-ββ-Induced Proliferation and Migration of VSMCs Through the G0/G1 Cell Cycle Arrest and Suppression of Activated PDGFRβ-PI3K-Akt Signaling Cascade

Fermented soshiho-tang with Lactobacillus plantarum enhances the antiproliferative activity in vascular smooth muscle cell

5,8-Dimethoxy-2-Nonylamino-Naphthalene-1,4-Dione Inhibits Vascular Smooth Muscle Cell Proliferation by Blocking Autophosphorylation of PDGF-Receptor β

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