Inhibitory effects of roscovitine on proliferation and migration of vascular smooth muscle cells in vitro

Zhang, Shuang-shuang; Wang, Wei; Zhao, Chongqiang; Xie, Mingxing; Li, Wenyu; Yang, Xiangli; Lv, Jiagao

doi:10.1007/s11596-014-1354-5

Cited by 10 publications

(8 citation statements)

References 36 publications

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“…The restenosis rate of 10%-20% after DES treatment of ASCVD remains a challenge for clinicians (3). Proliferation and migration of VSMCs and delayed endothelialization are believed to be the main pathological causes of in-stent restenosis (27). The results of this study revealed that paclitaxel hirudin complexes had a higher inhibition rate than the paclitaxel only treatment, suggesting that natural herbs have the capacity to enhance pharmacological effects.…”

Section: Discussionmentioning

confidence: 72%

Inhibitory Effects of Paclitaxel Hirudin Complexes on the Growth and Proliferation of Human Coronary Artery Smooth Muscle Cells and Endothelial Cells in Vitro: An Exploration of a New Type of Complex Monomer for Stents Eluting Natural Herbs

Li¹,

Wang²

2016

West Indian Med J

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Objective: To prove the effectiveness and feasibility of a paclitaxel hirudin complex and to provide experimental data on the prevention of restenosis, we investigated the effects of paclitaxel hirudin complexes on the growth of human coronary artery smooth muscle cells (HCASMCs) and endothelial cells (HCAECs) in vitro. Methods: HCASMCs and HCAECs were co-incubated with different concentrations of hirudin. Cell viability was assessed using methylthiazoletetrazolium (MTT) assays to determine the optimal concentration range for inhibiting the growth of HCASMCs but not that of HCAECs. Then, cells were incubated with hirudin within the optimal concentration range combined with 1 μmol/L paclitaxel. Results: Hirudin at 0.2-3.13 mg/mL significantly inhibited the growth of HCASMC (p < 0.05) but not HCAEC (p > 0.05) compared to the control group. This range of hirudin complexed with 1 µmol/L paclitaxel noticeably inhibited the growth of HCASMC (p < 0.05). Moreover, 1 μmol/L paclitaxel+0.39 mg/mL hirudin noticeably decreased the inhibition ratio of the growth of HCAECs compared with the paclitaxel only group (p < 0.05). The complex of 1 μmol/L paclitaxel plus 0.39 mg/mL hirudin can maximize the inhibition of HCASMCs and minimum the inhibition of HCAECs. Conclusions: The results of this study may provide reference data for the subsequent development of natural herb-eluting stents.

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Section: Discussionmentioning

confidence: 72%

Inhibitory Effects of Paclitaxel Hirudin Complexes on the Growth and Proliferation of Human Coronary Artery Smooth Muscle Cells and Endothelial Cells in Vitro: An Exploration of a New Type of Complex Monomer for Stents Eluting Natural Herbs

Li¹,

Wang²

2016

West Indian Med J

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“…Moreover, the MMP pathway can activate the caspase family members, leading to cell apoptosis and increase TNF-α 44 . In turn, TNF-α induces the proliferation of the HASMCs and the expression of MMP2 and MMP9 45 , 46 . RIP3 is involved in TNF-α-induced cell necrosis in SMCs 25 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-513b-5p targets COL1A1 and COL1A2 associated with the formation and rupture of intracranial aneurysm

Zhang

Chen

Wang

et al. 2021

Sci Rep

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Collagen-type I alpha 1 chain (COL1A1) and COL1A2 are abnormally expressed in intracranial aneurysm (IA), but their mechanism of action remains unclear. This study was performed to investigate the mechanism of COL1A1 and COL1A2 affecting the occurrence and rupture of IA. Quantitative real-time polymerase chain reaction was used to measure the expression of hsa-miR-513b-5p, COL1A1, COL1A2, TNF-α, IL-6, MMP2, MMP3, MMP9 and TIMP4 in patients with ruptured IA (RA) (n = 100), patients with un-ruptured IA (UA) (n = 100), and controls (n = 100). Then, human vascular smooth muscle cells (HASMCs) were cultured, and dual luciferase reporter assay was performed to analyse the targeting relationship between miR-513b-5p and COL1A1 or COL1A2. The effects of the miR-513b-5p mimic and inhibitor on the proliferation, apoptosis, and death of HASMC and the RIP1-RIP3-MLKL and matrix metalloproteinase pathways were also explored. The effect of silencing and over-expression of COL1A1 and COL1A2 on the role of miR-513b-5p were also evaluated. Finally, the effects of TNF-α on miR-513b-5p targeting COL1A1 and COL1A2 were tested. Compared with those in the control group, the serum mRNA levels of miR-513b-5p, IL-6 and TIMP4 were significantly decreased in the RA and UA groups, but COL1A1, COL1A2, TNF-α, IL-1β, MMP2, MMP3 and MMP9 were significantly increased (p < 0.05). Compared with those in the UA group, the expression of COL1A1, COL1A2, TNF-α, IL-1β and MMP9 was significantly up-regulated in the RA group (p < 0.05). Results from the luciferase reporter assay showed that COL1A1 and COL1A were the direct targets of miR-513b-5p. Further studies demonstrated that miR-513b-5p targeted COL1A1/2 to regulate the RIP1-RIP3-MLKL and MMP pathways, thereby enhancing cell death and apoptosis. Over-expression of COL1A1 or COL1A2, rather than silencing COL1A1/2, could improve the inhibitory effect of miR-513b-5p on cell activity by regulating the RIP1-RIP3-MLKL and MMP pathways. Furthermore, over-expression of miR-513b-5p and/or silencing COL1A1/2 inhibited the TNF-α-induced cell proliferation and enhanced the TNF-α-induced cell death and apoptosis. The mechanism may be related to the inhibition of collagen I and TIMP4 expression and promotion of the expression of RIP1, p-RIP1, p-RIP3, p-MLKL, MMP2 and MMP9. MiR-513b-5p targeted the inhibition of COL1A1/2 expression and affected HASMC viability and extracellular mechanism remodelling by regulating the RIP1-RIP3-MLKL and MMP pathways. This process might be involved in the formation and rupture of IA.

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“…In this project HASMCs were also stimulated with 50 ng/ml TNF-α, which is known to induce endogenous production of H 2 O 2 [ 30 – 32 ]. The results obtained here did not show any significant differences in MMP-2 and TIMP-1 mRNA quantity or protein secretion in comparison to untreated control cells.…”

Section: Discussionmentioning

confidence: 99%

Assessment of the correlation between oxidative stress and expression of MMP-2, TIMP-1 and COX-2 in human aortic smooth muscle cells

Oszajca

Szemraj

2021

Arch Med Sci Atheroscler Dis

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IntroductionSmooth muscle cells (SMCs) are considered to be the main producer of matrix metalloproteinase-2 (MMP-2) participating primarily in extracellular matrix (ECM) remodeling. Any disturbances in ECM structure may underlie the pathogenesis of many cardiovascular diseases and contribute to angiogenesis, cancer development, invasion or metastasis. The purpose of the study was to examine the effect of oxidative stress on the expression of MMP-2, its tissue inhibitor type 1 (TIMP-1) and cyclooxygenase-2 (COX-2) in human aortic smooth muscle cells (HASMCs).Material and methodsHASMCs were treated with exogenously applied H2O2 or TNF-α. N-acetylcysteine (NAC) was used as an antioxidant. Gene expression levels were measured by real-time PCR and the protein levels were determined using ELISA assay.ResultsThe studies revealed no association between oxidative stress and either mRNA quantity or protein secretion of MMP-2 and TIMP-1. However, we found markedly reduced (p < 0.001) MMP-2 secretion in cells incubated with NAC. HASMCs stimulated with TNF-α demonstrated a significantly increased COX-2 mRNA level as well as enzyme activity. H2O2-induced cells showed lowered COX-2 activity in comparison to untreated cells. MMP-2 and TIMP-1 expression did not change after COX-2 inhibition with DuP-697.ConclusionsWe did not find any effect of oxidative stress on expression of MMP-2 and TIMP-1 in HASMCs. However, COX-2 mRNA and protein level were elevated in these conditions. There was no correlation between COX-2 activity and MMP-2 and TIMP-1 mRNA expression or protein secretion.

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Inhibitory effects of roscovitine on proliferation and migration of vascular smooth muscle cells in vitro

Cited by 10 publications

References 36 publications

Inhibitory Effects of Paclitaxel Hirudin Complexes on the Growth and Proliferation of Human Coronary Artery Smooth Muscle Cells and Endothelial Cells in Vitro: An Exploration of a New Type of Complex Monomer for Stents Eluting Natural Herbs

Inhibitory Effects of Paclitaxel Hirudin Complexes on the Growth and Proliferation of Human Coronary Artery Smooth Muscle Cells and Endothelial Cells in Vitro: An Exploration of a New Type of Complex Monomer for Stents Eluting Natural Herbs

MicroRNA-513b-5p targets COL1A1 and COL1A2 associated with the formation and rupture of intracranial aneurysm

Assessment of the correlation between oxidative stress and expression of MMP-2, TIMP-1 and COX-2 in human aortic smooth muscle cells

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