Calcification of vascular smooth muscle cells is induced by secondary calciprotein particles and enhanced by tumor necrosis factor-α

Aghagolzadeh, Parisa; Bachtler, Matthias; Bijarnia, Rakesh Kumar; Jackson, Christopher B.; Smith, Edwin R.; Odermatt, Alex; Radpour, Ramin; Pasch, Andreas

doi:10.1016/j.atherosclerosis.2016.05.044

Cited by 201 publications

(226 citation statements)

References 48 publications

(64 reference statements)

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“…Inflammatory cytokines such as TNF-α may induce exosome secretion from VSMCs and thereby increase the procalcific properties of serum [57, 58]. Therefore, reducing the levels of pro-inflammatory molecules may limit the progression of vascular calcification [54-56, 59, 60]. …”

Section: Discussionmentioning

confidence: 99%

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Expanded Haemodialysis Therapy of Chronic Haemodialysis Patients Prevents Calcification and Apoptosis of Vascular Smooth Muscle Cells in vitro

et al. 2017

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Background: Vascular calcification is a common phenomenon in patients with chronic kidney disease and strongly associated with increased cardiovascular mortality. Vascular calcification is an active process mediated in part by inflammatory processes in vascular smooth muscle cells (VSMC). These could be modified by the insufficient removal of proinflammatory cytokines through conventional high-flux (HF) membranes. Recent trials demonstrated a reduction of inflammation in VSMC by use of dialysis membranes with a higher and steeper cut-off. These membranes caused significant albumin loss. Therefore, the effect of high retention Onset (HRO) dialysis membranes on vascular calcification and its implications in vitro was evaluated. Methods: In the PERCI II trial, 48 chronic dialysis patients were dialyzed using HF and HRO dialyzers and serum samples were collected. Calcifying VSMC were incubated with the serum samples. Calcification was determined using alizarin red staining (AZR) and determination of alkaline phosphatase (ALP) activity. Furthermore, apoptosis was evaluated, and release of matrix Gla protein (MGP), osteopontin (OPN) and growth differentiation factor 15 (GDF-15) were measured in cell supernatants. Results: Vascular calcification in vitro was significantly reduced by 24% (ALP) and 36% (AZR) after 4 weeks of HRO dialysis and by 33% (ALP) and 48% (AZR) after 12 weeks of dialysis using HRO membranes compared to HF dialysis. Apoptosis was significantly lower in the HRO group. The concentrations of MGP and OPN were significantly elevated after incubation with HF serum compared to HRO serum and healthy controls. Similarly, GDF-15 release in the supernatant was elevated after incubation with HF serum, an effect significantly ameliorated after treatment with HRO medium. Conclusions: Expanded haemodialysis therapy reduces the pro-calcific potential of serum from dialysis patients in vitro. With a markedly reduced albumin filtration compared to high cut-off dialysis, use of the HRO dialyzers may possibly provide a treatment option for chronic dialysis patients to reduce the progression of vascular calcification.

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Section: Discussionmentioning

confidence: 99%

“…IL-6 [52, 53], TNF-α [54-56] and VCAM [22] have been discussed as key inducers of vascular calcification. Hence, reducing these molecules may provide a possible explanation for the observed effects on VSMC calcification.…”

Section: Discussionmentioning

confidence: 99%

Expanded Haemodialysis Therapy of Chronic Haemodialysis Patients Prevents Calcification and Apoptosis of Vascular Smooth Muscle Cells in vitro

et al. 2017

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“…Primary CPP is considered to inhibit crystal growth and aggregation [44], but it undergo spontaneous maturation and develop crystalline structures to form secondary CPP. Aghagolzadeh et al have recently reported that secondary CPP has a potential to induce vascular calcification [45]. In addition, CPP maturation time (T 50 ) has been reported as an independent predictor of mortality in HD patients [46] and renal transplant recipients [47].…”

Section: Mg and Dialysis Therapymentioning

confidence: 99%

Cardiovascular disease, mortality, and magnesium in chronic kidney disease: growing interest in magnesium-related interventions

Ikee¹

2018

Ren Replace Ther

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Magnesium (Mg) is an essential element that plays pivotal roles in a number of biological processes in the human body. Hypomagnesemia is involved in the pathophysiology of hypertension, vascular calcification, and metabolic derangements including diabetes mellitus and dyslipidemia, which are all risk factors for cardiovascular disease, the leading cause of mortality and morbidity in patients with chronic kidney disease (CKD). Hypomagnesemia is also associated with the development and progression of CKD. As CKD advances, renal Mg excretion decreases and hypermagnesemia emerges in end-stage renal disease (ESRD). In addition, dialysates with high Mg concentrations, which were used in the early era of dialysis therapy, increased the risk of hypermagnesemia, and thus, the dialysate Mg composition has since been reduced. Accordingly, dialysis patients in the modern era commonly have normomagnesemia or even hypomagnesemia. The relationships between hypomagnesemia and cardiovascular disease and mortality have been increasingly reported in observational studies in CKD/ESRD. However, these relationships may be attenuated by a patient's race or region. Although dialysates with higher Mg concentrations or Mg-containing phosphate binders appear to be promising in this setting, only a few interventional studies have examined the effects of Mg supplementation on cardiovascular lesions. Furthermore, the effects of Mg supplementation on mortality have not yet been investigated as a primary end-point in randomized controlled trials. Further studies are required in order to establish the efficacy and safety of Mg in CKD patients.

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“…Vascular calcification in patients with CKD occurs via osteoblastic-like cell differentiation of the vascular smooth muscle cells in the kidneys. Some studies reported that cyclic adenosine monophosphate, which is mediated by tumor necrosis factor-α, stimulates the osteoblastic differentiation of vascular smooth muscle cells in kidney [36, 37]. In other studies, high extracellular calcium and phosphate concentrations have induced the transformation of vascular smooth muscle cells into osteoblast-like cells and accelerated the processes of active vascular calcification [38, 39].…”

Section: Discussionmentioning

confidence: 99%

The Relationship Between Pulse Pressure, the Estimated Glomerular Filtration Rate, and Urine Microalbumin/Creatinine Ratio in Korean Adults

Seong

Park

et al. 2017

Kidney Blood Press Res

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Background/Aims: Pulse pressure (PP) is a predictor of adverse outcomes in patients on haemodialysis. Thus, the present study was conducted to assess the relationship between PP, estimated glomerular filtration rate (eGFR), and urine microalbumin/creatinine ratio (uACR) in Korean adults. Methods: Data of 9,409 adults (4,206 men and 5,203 women) aged ≥ 20 years from the Sixth Korean National Health and Nutrition Examination Survey (2013–2014) were analyzed. Results: A multivariate analysis revealed that systolic blood pressure (SBP) (β = -0.170, 95% confidence interval [CI], -0.216 to -0.159), diastolic blood pressure (DBP) (β = 0.088, 95% CI 0.108–0.200; p < 0.001), and PP (β = -0.134, 95% CI -0.215 to -0.157) were significant factors determining eGFR. In contrast, SBP (β = 0.152, 95% CI, 0.985–1.456; p < 0.001), DBP (β = -0.062, 95% CI -1.141 to -0.442; p < 0.001), and PP (β = 0.118, 95% CI 0.965–1.436; p < 0.001) were the significant factors determining uACR. The odds ratios (ORs) of a high PP (PP ≥ 60 mmHg) with a normal group [eGFR ≥ 60 ml/min/1.73 m² and uACR < 30 mg/g] as a reference were significant for decreased eGFR [eGFR < 60 ml/min/1.73 m², 1.484 (95% CI, 1.003–2.196)], elevated uACR [uACR ≥ 30 mg/g, 2.592 (95% CI, 2.085–3.223)], and decreased eGFR plus elevated uACR [eGFR < 60 ml/min/1.73 m² and uACR ≥ 30 mg/g, 3.889 (95% CI, 2.519–6.004)]. Conclusion: Enhanced PP was associated with a decreased eGFR and an increase in uACR in Korean adults. In addition, the PP increased greatly when a decrease in eGFR and an increase in uACR appeared simultaneously.

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Calcification of vascular smooth muscle cells is induced by secondary calciprotein particles and enhanced by tumor necrosis factor-α

Abstract: Secondary, but not primary CPP, induce VSMC calcification. Secondary CPP induce the expression and release of TNF-α, which enhances calcification via its receptor TNFR1.

Cited by 201 publications

References 48 publications

Expanded Haemodialysis Therapy of Chronic Haemodialysis Patients Prevents Calcification and Apoptosis of Vascular Smooth Muscle Cells in vitro

Expanded Haemodialysis Therapy of Chronic Haemodialysis Patients Prevents Calcification and Apoptosis of Vascular Smooth Muscle Cells in vitro

Cardiovascular disease, mortality, and magnesium in chronic kidney disease: growing interest in magnesium-related interventions

The Relationship Between Pulse Pressure, the Estimated Glomerular Filtration Rate, and Urine Microalbumin/Creatinine Ratio in Korean Adults

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