Oxidized Low-Density Lipoprotein Increases Bone Sialoprotein Expression in Vascular Smooth Muscle Cells Via Runt-Related Transcription Factor 2

Farrokhi, Effat; Chaleshtori, Morteza Hashemzadeh; Samani, Keihan Ghatreh

doi:10.1097/maj.0000000000000381

Cited by 24 publications

(10 citation statements)

References 20 publications

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“…ERK is a widely expressed protein kinase and an intracellular signaling molecule that is involved in cell proliferation (28). Previous studies have indicated that ox-LDL induces VSMC proliferation through activation of the ERK pathway (19,29,30). In line with these results, the present study revealed that the phosphorylation of ERK1/2 in VSMCs was enhanced by ox-LDL, which was inhibited by pre-treatment with icariin.…”

Section: Discussionsupporting

confidence: 88%

Icariin inhibits oxidized low-density lipoprotein-induced proliferation of vascular smooth muscle cells by suppressing activation of extracellular signal-regulated kinase 1/2 and expression of proliferating cell nuclear antigen

Liu

Yan

et al. 2016

Molecular Medicine Reports

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Icariin, a flavonoid isolated from the traditional Chinese herbal medicine Epimedium brevicornum Maxim, has been shown to possess anti-inflammatory, anti‑oxidant and anti-atherosclerotic activities in vivo and in vitro. The aim of the present study was to investigate the effects of icariin on oxidized low‑density lipoprotein (ox-LDL)-induced proliferation of vascular smooth muscle cells (VSMCs) and the possible underlying mechanism. VSMCs were cultured and pre‑treated with various concentrations of icariin (0, 10, 20 or 40 µm) prior to stimulation by ox‑LDL (50 µg/ml). Cell proliferation was evaluated by an MTT assay. Flow cytometry was used to study the influence of icariin on the cell cycle. Proliferating cell nuclear antigen (PCNA) expression and phosphorylation levels of extracellular signal-regulated kinase (ERK)1/2 were detected by western blot analysis. The results indicated that icariin significantly inhibited ox‑LDL‑induced proliferation of VSMCs and phosphorylation of ERK1/2. Furthermore, icariin also blocked the ox‑LDL‑induced cell‑cycle progression at G1/S‑interphase and downregulated the expression of PCNA in VSMCs. In conclusion, the present study indicated for the first time that icariin reduced the amount of ox‑LDL‑induced proliferation of VSMCs through suppression of PCNA expression and inactivation of ERK1/2.

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Section: Discussionsupporting

confidence: 88%

Icariin inhibits oxidized low-density lipoprotein-induced proliferation of vascular smooth muscle cells by suppressing activation of extracellular signal-regulated kinase 1/2 and expression of proliferating cell nuclear antigen

Liu

Yan

et al. 2016

Molecular Medicine Reports

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“… 87 The resulting oxidative products may activate the NF-κB-RankL pathways provoking the production of procalcific cytokines, such as TNFα, IL-6, and IL-1β, 102–104 or induce mitochondrial DNA damage 87 and apoptosis of surrounding cells, such as VSMCs, 87 both of which contribute to the development of AIC. Indeed, exposure of VSMCs to oxLDL or hydrogen peroxide were found to induce osteoblastic differentiation of these cells 48 , 110 , 111 , likely mediated through the osteochondrogenic transcription factor Runx2 via AKT signalling. 48 Finally, in a mouse model of atherosclerosis, global knockout of Nox2 nicotinamide adenine dinucleotide phosphate (NADPH) oxidase markedly reduced aortic superoxide production and plaque size, 112 highlighting of the importance of ROS in atherogenesis.…”

Section: Arterial Intimal Calcificationmentioning

confidence: 99%

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

Durham

Speer

Scatena

et al. 2018

Cardiovascular Research

775

662

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Vascular calcification is associated with a significant increase in all-cause mortality and atherosclerotic plaque rupture. Calcification has been determined to be an active process driven in part by vascular smooth muscle cell (VSMC) transdifferentiation within the vascular wall. Historically, VSMC phenotype switching has been viewed as binary, with the cells able to adopt a physiological contractile phenotype or an alternate ‘synthetic’ phenotype in response to injury. More recent work, including lineage tracing has however revealed that VSMCs are able to adopt a number of phenotypes, including calcific (osteogenic, chondrocytic, and osteoclastic), adipogenic, and macrophagic phenotypes. Whilst the mechanisms that drive VSMC differentiation are still being elucidated it is becoming clear that medial calcification may differ in several ways from the intimal calcification seen in atherosclerotic lesions, including risk factors and specific drivers for VSMC phenotype changes and calcification. This article aims to compare and contrast the role of VSMCs in driving calcification in both atherosclerosis and in the vessel media focusing on the major drivers of calcification, including aging, uraemia, mechanical stress, oxidative stress, and inflammation. The review also discusses novel findings that have also brought attention to specific pro- and anti-calcifying proteins, extracellular vesicles, mitochondrial dysfunction, and a uraemic milieu as major determinants of vascular calcification.

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“…Of note, oxidative stress modulates osteogenic differentiation of vascular cells and bone cells in an opposite manner [128], [153], increasing VSMC calcification but inhibiting osteoblast differentiation. In VSMC, increased oxidative stress converted LDL into OxLDL, which promoted VSMC calcification [154]. In contrast, minimally oxidized low-density lipoprotein (mmLDL) and H 2 O 2 increased intracellular oxidative stress and inhibited osteogenic differentiation of pre-osteoblasts or bone marrow stromal cells [128].…”

Section: Regulation Of H2o2 Production In Vsmcmentioning

confidence: 99%

Redox signaling in cardiovascular pathophysiology: A focus on hydrogen peroxide and vascular smooth muscle cells

2016

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Oxidative stress represents excessive intracellular levels of reactive oxygen species (ROS), which plays a major role in the pathogenesis of cardiovascular disease. Besides having a critical impact on the development and progression of vascular pathologies including atherosclerosis and diabetic vasculopathy, oxidative stress also regulates physiological signaling processes. As a cell permeable ROS generated by cellular metabolism involved in intracellular signaling, hydrogen peroxide (H2O2) exerts tremendous impact on cardiovascular pathophysiology. Under pathological conditions, increased oxidase activities and/or impaired antioxidant systems results in uncontrolled production of ROS. In a pro-oxidant environment, vascular smooth muscle cells (VSMC) undergo phenotypic changes which can lead to the development of vascular dysfunction such as vascular inflammation and calcification. Investigations are ongoing to elucidate the mechanisms for cardiovascular disorders induced by oxidative stress. This review mainly focuses on the role of H2O2 in regulating physiological and pathological signals in VSMC.

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Oxidized Low-Density Lipoprotein Increases Bone Sialoprotein Expression in Vascular Smooth Muscle Cells Via Runt-Related Transcription Factor 2

Cited by 24 publications

References 20 publications

Icariin inhibits oxidized low-density lipoprotein-induced proliferation of vascular smooth muscle cells by suppressing activation of extracellular signal-regulated kinase 1/2 and expression of proliferating cell nuclear antigen

Icariin inhibits oxidized low-density lipoprotein-induced proliferation of vascular smooth muscle cells by suppressing activation of extracellular signal-regulated kinase 1/2 and expression of proliferating cell nuclear antigen

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

Redox signaling in cardiovascular pathophysiology: A focus on hydrogen peroxide and vascular smooth muscle cells

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