Para‐cresyl sulfate acutely impairs vascular reactivity and induces vascular remodeling

Gross, Priscilla; Massy, Ziad A.; Hénaut, Lucie; Boudot, Cédric; Cagnard, Joanna; March, Cécilia; Kamel, Saı̈d; Drueke, Tilman B.; Six, Isabelle

doi:10.1002/jcp.25018

Cited by 60 publications

(44 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To the best of our knowledge, no previous study has tried to correlate the expression of these toxins with serum miRNA levels in CKD patients. Interestingly, miR-126 expression was correlated with PCS and IS, which could be related to the fact that miR-126 is an endothelial-specific miRNA, associated with endothelial dysfunction [32, 33]. On the other hand, IS was also correlated with miR-143 and miR-155, while IAA was not correlated with any miRNA.…”

Section: Discussionmentioning

confidence: 99%

Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

et al. 2016

Self Cite

View full text Add to dashboard Cite

BackgroundMicroRNAs (miRNAs) are innovative and informative blood-based biomarkers involved in numerous pathophysiological processes. In this study and based on our previous experimental data, we investigated miR-126, miR-143, miR-145, miR-155 and miR-223 as potential circulating biomarkers for the diagnosis and prognosis of patients with chronic kidney disease (CKD). The primary objective of this study was to assess the levels of miRNA expression at various stages of CKD.MethodsRNA was extracted from serum, and RT-qPCR was performed for the five miRNAs and cel-miR-39 (internal control).ResultsSerum levels of miR-143, -145 and -223 were elevated in patients with CKD compared with healthy controls. They were further increased in chronic haemodialysis patients, but were below control levels in renal transplant recipients. In contrast, circulating levels of miR-126 and miR-155 levels, which were also elevated in CKD patients, were lower in the haemodialysis group and even lower in the transplant group. Four of the five miRNA species were correlated with estimated glomerular filtration rate, and three were correlated with circulating uraemic toxins.ConclusionsThis exploratory study suggests that specific miRNAs could be biomarkers for complications of CKD, justifying further studies to link changes of miRNA levels with outcomes in CKD patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

et al. 2016

Self Cite

View full text Add to dashboard Cite

show abstract

“…Açaí fruits from the Amazon region (Belém do Pará, Brazil, 2 • 57 ′ 29,47 ″ S/47 • 23 ′ 10,37 ″ W) were processed to obtain the hydro-alcoholic extract as previously described (Rocha et al 2007 HUVECs preserve endothelial cell native characteristics, including the expression of specific surface markers and intracellular signalling pathways. HUVECs were chosen as an experimental model in this study, since they have been a useful model to investigate endothelial dysfunction promoted by uraemic toxins (Dou et al 2004(Dou et al , 2007Faure et al 2006;Gross et al 2015;Lu et al 2016;Migliori et al 2015) and also other biological actions (Addi et al 2019;Shen et al 2016).…”

Section: Açaí Seed Extractmentioning

confidence: 99%

Uraemic toxin‐induced inflammation and oxidative stress in human endothelial cells: protective effect of polyphenol‐rich extract from açaí

Monteiro

Soares

Trindade

et al. 2020

Experimental Physiology

View full text Add to dashboard Cite

New Findings What is the central question of this study?Does a polyphenol‐rich extract from açaí have a potential role in preventing uraemic toxin‐induced endothelial cell dysfunction? What is the main finding and its importance?Polyphenols from açaí prevented cell death, restored migratory capacity, protected from inflammation and contributed to the restoration of the antioxidant response in endothelial cells exposed to uraemic toxins. The protective role of açaí against toxic effects exerted by uraemic toxins presents a potential new therapeutic target in endothelial cells. Abstract In chronic kidney disease (CKD), progressive loss of kidney function results in the accumulation of protein‐bound uraemic toxins such as p‐cresyl sulfate (pCS) and indoxyl sulfate (IS). Among strategies to ameliorate the harmful actions of uraemic toxins, phenolic compounds have been extensively studied. The main goal of this work was to evaluate the antioxidant and anti‐inflammatory actions of phenolic‐rich açaí seed extract (ASE) in response to endothelial dysfunction induced by IS and pCS, in human umbilical vein endothelial cells (HUVECs). Cells were treated with ASE (10 µg ml−1) in the presence or absence of IS (61 µg ml−1) and pCS (40 µg ml−1). Cell viability, cell death, cell migratory capacity and inflammatory biomarker expression were evaluated. Cellular antioxidant response was measured through the activity and expression of antioxidant enzymes, and oxidative damage was evaluated. IS and pCS lowered cell viability, triggered cell death and lowered the migratory capacity in endothelial cells (P < 0.05). ASE prevented cell death and restored the migratory capacity in cells exposed to IS. Both toxins up‐regulated pro‐inflammatory cytokine expression, and ASE was able to beneficially counteract this effect. Tumour necrosis factor‐α secretion was greater in uraemic toxin‐treated cells and ASE reversed this phenomenon in cells treated with both toxins concomitantly (P < 0.05). With regard to the antioxidant response, superoxide dismutase expression was strikingly lower in cells treated with both toxins, and ASE inhibited this harmful effect (P < 0.05). From the results, we conclude that ASE exerted protective effects on inflammation and oxidative stress caused by uraemic toxins (particularly by IS) in human endothelial cells.

show abstract

“…In mouse aortic segments, implemented preloads are highly variable among different studies and range from about 1.2–8.0 mN/mm (Fransen et al, 2008, 2015; Van Hove et al, 2009; Ponnoth et al, 2012; van Langen et al, 2012; Lloyd et al, 2013; Taguchi et al, 2014; Gross et al, 2015; Leloup et al, 2015a; Zhou et al, 2015). According to Laplace's law, and assuming a thin, isotropic and homologous wall for large vessels such as the aorta, the transmural pressure (P, in mm Hg) is directly proportional to the preload (PL, in mN) and inversely proportional to its length (l, in mm) and radius (r, in mm): P = PL/(l × 2r) × 7.5) (Syyong et al, 2009; Van Herck et al, 2009; Butlin et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Isometric Stretch Alters Vascular Reactivity of Mouse Aortic Segments

et al. 2017

View full text Add to dashboard Cite

Most vaso-reactive studies in mouse aortic segments are performed in isometric conditions and at an optimal preload, which is the preload corresponding to a maximal contraction by non-receptor or receptor-mediated stimulation. In general, this optimal preload ranges from about 1.2 to 8.0 mN/mm, which according to Laplace's law roughly correlates with transmural pressures of 10–65 mmHg. For physiologic transmural pressures around 100 mmHg, preloads of 15.0 mN/mm should be implemented. The present study aimed to compare vascular reactivity of 2 mm mouse (C57Bl6) aortic segments preloaded at optimal (8.0 mN/mm) vs. (patho) physiological (10.0–32.5 mN/mm) preload. Voltage-dependent contractions of aortic segments, induced by increasing extracellular K+, and contractions by α1-adrenergic stimulation with phenylephrine (PE) were studied at these preloads in the absence and presence of L-NAME to inhibit basal release of NO from endothelial cells (EC). In the absence of basal NO release and with higher than optimal preload, contractions evoked by depolarization or PE were attenuated, whereas in the presence of basal release of NO PE-, but not depolarization-induced contractions were preload-independent. Phasic contractions by PE, as measured in the absence of external Ca2+, were decreased at higher than optimal preload suggestive for a lower contractile SR Ca2+ content at physiological preload. Further, in the presence of external Ca2+, contractions by Ca2+ influx via voltage-dependent Ca2+ channels were preload-independent, whereas non-selective cation channel-mediated contractions were increased. The latter contractions were very sensitive to the basal release of NO, which itself seemed to be preload-independent. Relaxation by endogenous NO (acetylcholine) of aortic segments pre-contracted with PE was preload-independent, whereas relaxation by exogenous NO (diethylamine NONOate) displayed higher sensitivity at high preload. Results indicated that stretching aortic segments to higher than optimal preload depolarizes the SMC and causes Ca2+ unloading of the contractile SR, making them extremely sensitive to small changes in the basal release of NO from EC as can occur in hypertension or arterial stiffening.

show abstract

Para‐cresyl sulfate acutely impairs vascular reactivity and induces vascular remodeling

Cited by 60 publications

References 51 publications

Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

Serum microRNAs are altered in various stages of chronic kidney disease: a preliminary study

Uraemic toxin‐induced inflammation and oxidative stress in human endothelial cells: protective effect of polyphenol‐rich extract from açaí

Isometric Stretch Alters Vascular Reactivity of Mouse Aortic Segments

Contact Info

Product

Resources

About