Vascular smooth muscle cell phenotypic plasticity and the regulation of vascular calcification

Iyemere, Valentine P.; Proudfoot, Diane; Weissberg, Peter L.; Shanahan, Catherine M.

doi:10.1111/j.1365-2796.2006.01692.x

Cited by 210 publications

(170 citation statements)

References 127 publications

(150 reference statements)

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“…In rodents, warfarin treatment induces rapid VC and decreased arterial compliance (5,6) akin to elastocalcinosis, a condition prevalent in the elderly population and characterized by calcium deposition along the elastic lamellae. Extensive research over the past decades has established that VC is at least in part a cell-mediated process that includes stimulation of osteogenic/chondrogenic differentiation in vascular smooth muscle (7,8), vesicle release, apoptosis, extracellular matrix degradation, and loss of calcification inhibitors (9,10).…”

Section: Vascular Calcification (Vc)mentioning

confidence: 99%

Quercetin Attenuates Warfarin-induced Vascular Calcification in Vitro Independently from Matrix Gla Protein

Beazley

Eghtesad

Nurminskaya

2013

Journal of Biological Chemistry

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Background: Molecular mechanism(s) of warfarin-induced vascular calcification are not well known. Results: Inhibition of ␤-catenin signaling with shRNA or quercetin prevents osteoblastic transformation and calcification in VSMCs and calcification in aortic rings treated with warfarin, independent from MGP and protein carboxylation. Conclusion: Quercetin inhibits vascular calcification via ␤-catenin signaling. Significance: Quercetin may be instrumental in treatment of warfarin-induced vascular calcification.

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Section: Vascular Calcification (Vc)mentioning

confidence: 99%

Quercetin Attenuates Warfarin-induced Vascular Calcification in Vitro Independently from Matrix Gla Protein

Beazley

Eghtesad

Nurminskaya

2013

Journal of Biological Chemistry

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“…Smooth muscle cells have been used as an effective model for studying vascular calcification in vitro [3] . However, there are other kinds of cells that also contribute to vascular pathology.…”

Section: Introductionmentioning

confidence: 99%

Oxidized low-density lipoprotein and β-glycerophosphate synergistically induce endothelial progenitor cell ossification

Liu

Chen

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the ability of ox-LDL to induce ossification of endothelial progenitor cells (EPCs) in vitro and explored whether oxidative stress, especially hypoxia inducible factor-1α (HIF-1α) and reactive oxygen species (ROS), participate in the ossific process. Methods: Rat bone marrow-derived endothelial progenitor cells (BMEPCs) were cultured in endothelial growth medium supplemented with VEGF (40 ng/mL) and bFGF (10 ng/mL). The cells were treated with oxidized low-density lipoprotein (ox-LDL, 5 µg/mL) and/or β-glycerophosphate (β-GP, 10 mmol/L). Calcium content and Von Kossa staining were used as the measures of calcium deposition. Ossific gene expression was determined using RT-PCR. The expression of osteocalcin (OCN) was detected with immunofluorescence. Alkaline phosphatase (ALP) activity was analyzed using colorimetric assay. Intercellular reactive oxygen species (ROS) were measured with flow cytometry. Results: BMEPCs exhibited a spindle-like shape. The percentage of cells that expressed the cell markers of EPCs CD34, CD133, and kinase insert domain-containing receptor (KDR) were 46.2%±5.8%, 23.5%±4.0%, and 74.3%±8.8%, respectively. Among the total cells, 78.3%±4.2% were stained with endothelial-specific fluorescence. Treatment of BMEPCs with ox-LDL significantly promoted calcium deposition, which was further significantly enhanced by co-treatment with β-GP. The same treatments significantly increased the gene expression of core-binding factor a-1 (cbfa-1) and OCN, while decreased the gene expression of osteoprotegerin (OPG). The treatments also significantly enhanced the activity of ALP, but did not affect the number of OCN + cells. Furthermore, the treatments significantly increased ROS and activated the hypoxia inducible factor-1α (HIF-1α). In all these effects, ox-LDL acted synergistically with β-GP. Conclusion: Ox-LDL and β-GP synergistically induce ossification of BMEPCs, in which an oxidizing mechanism is involved.

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“…However, in presence of enhanced vascular damage due to persistent OS and/or hyperglycaemic milieu, the processes of phenotypic differentiation and regulation may be disconcerted, leading to abnormal differentiation and transformation of the VSMC into other mesenchymal lineages such as osteoblasts, chondrocytes and adipocytes, which facilitates processes of atherosclerosis and VC [38]. In addition to NADPH, Xanthine oxidase is a major contributor to increased OS in the vascular lumen and reduced NO levels, especially in type 2 DM subjects [10].…”

Section: Oxidative Stress and Vascular Calcificationmentioning

confidence: 99%

Vascular Calcification in Type 2 Diabetes: A Role for Allopurinol?

Singh¹,

Farrington²

2015

J Diabetes Metab

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Vascular calcification contributes significantly to the vascular damage burden in type 2 diabetes. Chronic hyperglycaemia is the driver of initiation and progression of vascular damage in these subjects. Enhanced oxidative stress is widespread in these subjects due to complex metabolic, cytokine, inflammatory and ageing factors, on the background of chronic hyperglycaemia. All these factors together contribute to an increased risk of vascular damage leading to atherosclerosis and vascular calcification. The xanthine oxidase system is a major contributor to the development of enhanced oxidative stress through generation of excessive free radicals. Current standard therapy is focused on controlling hyperglycaemia and screening/treatment of known co-morbidities. However, these therapies do not target oxidative stress. Allopurinol, a potent xanthine oxidase inhibitor has demonstrated beneficial effects on several parameters of vascular health such as reduction in oxidative stress, proteinuria, reversal of vascular damage, regression of ventricular hypertrophy and arresting the rate of progression of chronic kidney disease. A randomised clinical trial of Allopurinol for amelioration of oxidative stress, endothelial cell dysfunction and vascular calcification in subjects with type 2 DM may be helpful to explore its potential in this area.

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Vascular smooth muscle cell phenotypic plasticity and the regulation of vascular calcification

Abstract: Abstract. Iyemere VP, Proudfoot D, Weissberg PL, Shanahan CM. (University of Cambridge, UK). Vascular smooth muscle cell phenotypic plasticity and the regulation of vascular calcification (Review).

Cited by 210 publications

References 127 publications

Quercetin Attenuates Warfarin-induced Vascular Calcification in Vitro Independently from Matrix Gla Protein

Quercetin Attenuates Warfarin-induced Vascular Calcification in Vitro Independently from Matrix Gla Protein

Oxidized low-density lipoprotein and β-glycerophosphate synergistically induce endothelial progenitor cell ossification

Vascular Calcification in Type 2 Diabetes: A Role for Allopurinol?

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