JM91, a newly synthesized indoledione derivative, inhibits rat aortic vascular smooth muscle cells proliferation and cell cycle progression through inhibition of ERK1/2 and Akt activations

Seo, Ji-Min; Jin, Yong-Ri; Ryu, Chong Kul; Kim, Tack-Joong; Han, Xianghua; Jiang, Hong; Yoo, Hwan‐Soo; Lee, Chong-Kil; Yun, Young Won

doi:10.1016/j.bcp.2007.11.013

Cited by 11 publications

(6 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As shown in Figure 3, we observed that acerogenin C specifically inhibited PDGF-stimulated PLCγ1 and Akt activation but not PDGFR and ERK1/2 MAP kinase activation in HASMCs. These results are similar to a previous study, in which JM91 inhibited PDGF-induced PI3-K/Akt and ERK1/2 MAP kinase activation but not PDGF Rβ in HASMCs [12]. In the present study, PDGFRβ, PLCγ1, ERK1/2 and Akt were used as a control for protein loading.…”

Section: Discussionsupporting

confidence: 93%

“…The PDGF-BB-stimulated mitogenesis signaling pathway has been well characterized. Binding of PDGF-BB to PDGF-Rβ can activate three major signal transduction pathways, PI3-K/Akt, PLCγ1 and ERK1/2, by activating Raf-1 [12]. As shown Figure 3, acerogenin C had no effect on the PDGF-BB-induced phosphorylation of PDGF-Rβ at various concentrations.…”

Section: Discussionmentioning

confidence: 86%

“…It is well-known that binding of signal transduction molecules to different phosphorylated tyrosine residues in PDGF-Rβ and PDGF-BB triggers the PI3-K/PKB (Akt) and PLCγ1 pathways in addition to the ERK pathway [12]. PI3-K mediates many different cellular responses, including actin reorganization, chemotaxis, cell growth and the serine/threonine kinase Akt/PKB for the antiapoptotic effect [13]- [15].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Antiproliferative Activity of Acerogenin C, a Macrocyclicdiarylheptanoid, on PDGF-Induced Human Aortic Smooth Muscle Cells Proliferation

Cha

Shi²,

Watanabe³

et al. 2015

View full text Add to dashboard Cite

Platelet-derived growth factor (PDGF)-BB is one of the most potent factors in the development and progression of various vascular disorders, such as atherosclerosis and restenosis. PDGF is a major stimulant for vascular smooth muscle cells (VSMCs) proliferation via the mitogenesis signaling pathway. In the present study, we investigated the effect of acerogenin C, a macrocyclicdiarylheptanoid, on PDGF-BB-stimulated human aortic smooth muscle cells (HASMCs) proliferation. Acerogenin C significantly inhibited PDGF (20 ng/mL)-BB-induced [ 3 H]-thymidine incorporation into DNA at concentrations of 0.1, 1 and 10 µM without any cytotoxicity. Acerogenin C also blocked PDGF-BB-stimulated phosphorylation of PLCγ1 and Akt but had no effect on extracellular signalregulated kinase 1/2 (ERK1/2) and PDGF beta-receptor (Rβ) activation. In addition, acerogenin C (0.1-10 μM) induced cell-cycle arrest in the G 1 phase, which was associated with the down-regulation of cyclins and the up-regulation of p27 kip1. These results suggest that acerogenin C blocks PDGF-BB-stimulated HASMCs proliferation via G 0 /G 1 arrest in association with the induction of p27 kip1 and the suppression of PLCγ1 and phosphatidylinositol 3-kinase (PI3-K)/Akt signaling pathways. Furthermore, acerogenin C may be used for prevention and treatment of atherosclerosis during restenosis after coronary angioplasty.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Antiproliferative Activity of Acerogenin C, a Macrocyclicdiarylheptanoid, on PDGF-Induced Human Aortic Smooth Muscle Cells Proliferation

Cha

Shi²,

Watanabe³

et al. 2015

View full text Add to dashboard Cite

show abstract

“…After quiescent VSMCs had been treated with GA for an additional 24 hrs, the cell lysis was harvested at 5 minutes (ERK1/2, PLC-1) 28) and 15 minutes (AKT, JNK) 22,29) after stimulation with PDGF-BB (50 g/L). Western blotting results are shown in Fig.…”

Section: Effects Of Ga On Plc-1 Erk1/2 Pi3k/akt and Jnk Phosphorylamentioning

confidence: 99%

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor β Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells

Liu

et al. 2010

J Atheroscler Thromb

View full text Add to dashboard Cite

Aim: Gambogic acid (GA) is the major active compound of Gamboge, a brownish or orange resin exuded from Garcinia hanburryi tree in Southeast Asia. Previous studies have demonstrated that GA exhibits potent anticancer effects by inducing cell cycle arrest or apoptosis in many types of cancer cell lines and blocking angiogenesis via inhibition of vascular endothelial cell proliferation and migration. Proliferation and migration of vascular smooth muscle cells (VSMCs) are critical steps in the progress of atherosclerosis and restenosis after angioplasty. In the present study, we investigated whether GA has an inhibitory effect on the proliferation and migration of VSMCs and its possible mechanism. Methods: The inhibitory effect of GA on the proliferation induced by PDGF-BB and EGF was measured by using Cell number counting assay and [

show abstract

“…Early study of related QIDs reveals that the compounds induce the tumor cell apoptosis by cell cycle control, angiogenesis control or topoisomerase II inhibition (14-17). In this study, the induction of immunological death of colon cancer cells by EY-6 is observed to learn the scientific basis to develop the candidate materials for efficacious and safe anti-cancer drug.…”

Section: Introductionmentioning

confidence: 99%

Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell

Ryu

Baek

et al. 2011

Immune Netw

Self Cite

View full text Add to dashboard Cite

BackgroundEY-6 is one of the newly synthesized indoledione derivatives to induce tumor cell-specific cell death. In this study, we investigated the mechanism of immunological death induced by EY-6 at mouse colon cancer cell as well as at the normal immune cell represented by dendritic cell.MethodsC57BL/6 mouse syngeneic colon cancer cell MC38 was treated with EY-6, and analyzed by MTT for viability test, flow cytometry for confirming surface expressing molecules and ELISA for detection of cytokine secretion. Normal myeloid-dendritic cell (DC) was ex vivo cultured from bone marrow hematopoietic stem cells of C57BL/6 mice with GM-CSF and IL-4 to analyze the DC uptake of dead tumor cells and to observe the effect of EY-6 on the normal DC.ResultsEY-6 killed the MC38 tumor cells in a dose dependent manner (25, 50 and 100 µM) with carleticulin induction. And EY-6 induced the secretion of IFN-γ but not of TNF-α from the MC38 tumor cells. EY-6 did not kill the ex-vivo cultured DCs at the dose killing tumor cells and did slightly but not significantly induced the DC maturation. The OVA-specific cross-presentation ability of DC was not induced by chemical treatment (both MHC II and MHC I-restricted antigen presentation).ConclusionData indicate that the EY-6 induced tumor cell specific and immunological cell death by modulation of tumor cell phenotype and cytokine secretion favoring induction of specific immunity eliminating tumor cells.

show abstract

JM91, a newly synthesized indoledione derivative, inhibits rat aortic vascular smooth muscle cells proliferation and cell cycle progression through inhibition of ERK1/2 and Akt activations

Cited by 11 publications

References 41 publications

Antiproliferative Activity of Acerogenin C, a Macrocyclicdiarylheptanoid, on PDGF-Induced Human Aortic Smooth Muscle Cells Proliferation

Antiproliferative Activity of Acerogenin C, a Macrocyclicdiarylheptanoid, on PDGF-Induced Human Aortic Smooth Muscle Cells Proliferation

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor β Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells

Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell

Contact Info

Product

Resources

About

JM91, a newly synthesized indoledione derivative, inhibits rat aortic vascular smooth muscle cells proliferation and cell cycle progression through inhibition of ERK1/2 and Akt activations

Cited by 11 publications

References 41 publications

Antiproliferative Activity of Acerogenin C, a Macrocyclicdiarylheptanoid, on PDGF-Induced Human Aortic Smooth Muscle Cells Proliferation

Antiproliferative Activity of Acerogenin C, a Macrocyclicdiarylheptanoid, on PDGF-Induced Human Aortic Smooth Muscle Cells Proliferation

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor &beta; Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells

Cellular Mechanism of Newly Synthesized Indoledione Derivative-induced Immunological Death of Tumor Cell

Contact Info

Product

Resources

About

Gambogic Acid Induces G0/G1 Cell Cycle Arrest and Cell Migration Inhibition Via Suppressing PDGF Receptor β Tyrosine Phosphorylation and Rac1 Activity in Rat Aortic Smooth Muscle Cells