Mechanisms of post-intervention arterial remodelling

Goel, Shakti A.; Guo, Lian‐Wang; Liu, Bo; Kent, K. Craig

doi:10.1093/cvr/cvs276

Cited by 95 publications

(98 citation statements)

References 70 publications

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“…This can be considered an exaggerated form of wound healing characterized by luminal (re)narrowing due to smooth muscle hyperplasia and rapid vascular remodelling of the instrumented vessel [1]. The formation of neointima is a complex and multifactorial process, but excessive VSMC (vascular smooth muscle cell) proliferation and migration, inflammation and the production of large amounts of ECM (extracellular matrix) are all involved [2].…”

Section: Introductionmentioning

confidence: 99%

“…In a rabbit model of balloon injury, there is early upAbbreviations: 2-ClHDA, 2-chlorohexadecanal; ApoE, apolipoprotein E; BrdU, bromodeoxyuridine; DAB, 3,3-diaminobenzidine; ECM, extracellular matrix; FCS, fetal calf serum; i.p., intraperitoneal; LCA, left carotid artery; LDL, low-density lipoprotein; MPO, myeloperoxidase; oxLDL, oxidized low-density lipoprotein; PAPC, 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PGPC, 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine; POVPC, 1-palmitoyl-2-oxovaleroyl-sn-glycero-3-phosphocholine; PS, phosphatidylserine; RCA, right carotid arteries; SOPC, 1-stearoyl-2-oleoyl-sn-glycero-3-phosphocholine; VSMC, vascular smooth muscle cell; αSMA, α smooth muscle actin. 1 Correspondence: Simon Kennedy (e-mail simon.kennedy@glasgow.ac.uk).…”

Section: Introductionmentioning

confidence: 99%

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Differential effects of chlorinated and oxidized phospholipids in vascular tissue: implications for neointima formation

et al. 2015

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The presence of inflammatory cells and MPO (myeloperoxidase) in the arterial wall after vascular injury could increase neointima formation by modification of phospholipids. The present study investigates how these phospholipids, in particular oxidized and chlorinated species, are altered within injured vessels and how they affect VSMC (vascular smooth muscle cell) remodelling processes. Vascular injury was induced in C57BL/6 mice and high fat-fed ApoE −/− (apolipoprotein E) mice by wire denudation and ligation of the left carotid artery (LCA). Neointimal and medial composition was assessed using immunohistochemistry and ESI-MS. Primary rabbit aortic SMCs (smooth muscle cells) were utilized to examine the effects of modified lipids on VSMC proliferation, viability and migration at a cellular level. Neointimal area, measured as intima-to-media ratio, was significantly larger in wire-injured ApoE −/− mice (3.62 + − 0.49 compared with 0.83 + − 0.25 in C57BL/6 mice, n = 3) and there was increased oxidized low-density lipoprotein (oxLDL) infiltration and elevated plasma MPO levels. Relative increases in lysophosphatidylcholines and unsaturated phosphatidylcholines (PCs) were also observed in wire-injured ApoE −/− carotid arteries. Chlorinated lipids had no effect on VSMC proliferation, viability or migration whereas chronic incubation with oxidized phospholipids stimulated proliferation in the presence of fetal calf serum [154.8 + − 14.2 % of viable cells at 1 μM PGPC (1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine) compared with control, n = 6]. In conclusion, ApoE −/− mice with an inflammatory phenotype develop more neointima in wire-injured arteries and accumulation of oxidized lipids in the vessel wall may propagate this effect.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Differential effects of chlorinated and oxidized phospholipids in vascular tissue: implications for neointima formation

et al. 2015

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“…It is well known that a majority of patients undergo re-stenosis after the primary angioplasty procedures within 6 months of the treatment [10]. A number of laboratories have been working to understand the mechanism for the same.…”

Section: Role Of Insulin and Igfs In Vascular Restenosismentioning

confidence: 99%

“…In another in-vitro study, it has been shown that TGF beta and Smad3 treated smooth muscle cells (in vitro model for vascular injury) lead to increased secretion of CTGF and IGFII from vascular smooth muscle cells which in-turn stimulated collagen III more than Collagen I from vascular fibroblasts thus leading to adaptive vessel remodelling [4,10].…”

Section: Role Of Insulin and Igfs In Vascular Restenosismentioning

confidence: 99%

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Is Insulin like Growth Factor a new wonder drug?

Goel

2017

J Med Res Innov

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Cucurbitacins mitigate vascular neointimal hyperplasia by suppressing cyclin A2 expression and inhibiting VSMC proliferation

Yuan,

Qian,

et al. 2024

Anim Models and Exp Med

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BackgroundRestenosis frequently occurs after percutaneous angioplasty in patients with vascular occlusion and seriously threatens their health. Substantial evidence has revealed that preventing vascular smooth muscle cell proliferation using a drug‐eluting stent is an effective approach to improve restenosis. Cucurbitacins have been demonstrated to exert an anti‐proliferation effect in various tumors and a hypotensive effect. This study aims to investigate the role of cucurbitacins extracted from Cucumis melo L. (CuECs) and cucurbitacin B (CuB) on restenosis.MethodsC57BL/6 mice were subjected to left carotid artery ligation and subcutaneously injected with CuECs or CuB for 4 weeks. Hematoxylin–Eosin, immunofluorescence and immunohistochemistry staining were used to evaluate the effect of CuECs and CuB on neointimal hyperplasia. Western blot, real‐time PCR, flow cytometry analysis, EdU staining and cellular immunofluorescence assay were employed to measure the effects of CuECs and CuB on cell proliferation and the cell cycle in vitro. The potential interactions of CuECs with cyclin A2 were performed by molecular docking.ResultsThe results demonstrated that both CuECs and CuB exhibited significant inhibitory effects on neointimal hyperplasia and proliferation of vascular smooth muscle cells. Furthermore, CuECs and CuB mediated cell cycle arrest at the S phase. Autodocking analysis demonstrated that CuB, CuD, CuE and CuI had high binding energy for cyclin A2. Our study also showed that CuECs and CuB dramatically inhibited FBS‐induced cyclin A2 expression. Moreover, the expression of cyclin A2 in CuEC‐ and CuB‐treated neointima was downregulated.ConclusionsCuECs, especially CuB, exert an anti‐proliferation effect in VSMCs and may be potential drugs to prevent restenosis.

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Mechanisms of post-intervention arterial remodelling

Cited by 95 publications

References 70 publications

Differential effects of chlorinated and oxidized phospholipids in vascular tissue: implications for neointima formation

Differential effects of chlorinated and oxidized phospholipids in vascular tissue: implications for neointima formation

Is Insulin like Growth Factor a new wonder drug?

Cucurbitacins mitigate vascular neointimal hyperplasia by suppressing cyclin A2 expression and inhibiting VSMC proliferation

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