Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26236562_1.fastq.gz | Fastqsanger.gz | |||
| SRR26236562_2.fastq.gz | Fastqsanger.gz | |||
| SRR26236563_1.fastq.gz | Fastqsanger.gz | |||
| SRR26236563_2.fastq.gz | Fastqsanger.gz | |||
| SRR26236564_1.fastq.gz | Fastqsanger.gz |
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Project description:Chronic kidney disease (CKD) accelerates vascular calcification (VC) via phenotypic switching of vascular smooth muscle cells (VSMCs). We investigated the roles of circulating small extracellular vesicles (sEVs) between the kidneys and VSMCs and uncovered relevant sEV-propagated microRNAs (miRNAs) and their biological signaling pathways. We established CKD models in rats and mice by adenine-induced tubulointerstitial fibrosis. The miRNA transcriptome of sEVs revealed a depletion of several miRNAs in CKD. Their expression levels in sEVs from CKD patients were correlated to kidney function. This study revealed the transcriptomic landscape of miRNAs propagated in sEVs in CKD. We investigated the therapeutic potential of miRNAs in VC.
2022-12-31 | GSE217558 | GEO
Project description:Background: Vascular calcification (VC) is a severe complication of chronic kidney disease (CKD) and increases cardiovascular morbidity and mortality. Extracellular vesicles (EVs) from bone mesenchymal stem cells (BMSCs) may influence vascular health through intercellular communication. This study investigated how CKD alters the anti-calcific function of BMSC-derived EVs, focusing on microRNA content, particularly miR-29a-3p. Methods: EVs were isolated from healthy and CKD-affected BMSCs and assessed for size, uptake by vascular smooth muscle cells (VSMCs), and miRNA content. High-phosphate-treated VSMCs and CKD rat models of vascular calcification were used to evaluate the effects of EVs on VC. Circulating miR-29a-3p was measured in hemodialysis patients and correlated with VC severity. Results: EVs from both groups showed comparable size and VSMC uptake. However, CKD-derived EVs had an altered miRNA profile, including markedly reduced miR-29a-3p, and showed diminished ability to inhibit phosphate-induced calcification. Restoration of miR-29a-3p suppressed calcification in vitro and in vivo. In hemodialysis patients, circulating miR-29a-3p was inversely associated with calcification severity. Conclusions: CKD impairs the anti-calcific function of BMSC-derived EVs partly through downregulation of EV-associated miR-29a-3p. Restoring miR-29a-3p may help mitigate VC in CKD, and circulating miR-29a-3p may serve as a clinical biomarker.
2026-07-01 | GSE301484 | GEO
Project description:Hyponatremia, one of the most frequently observed electrolyte disorders in patients with chronic kidney disease (CKD), is associated with increased mortality. Lower sodium concentrations or low osmolar conditions are shown to induce cell damages via apoptosis and oxidative stress, both of accelerate vascular calcification (VC), a critical phenotype of CKD patients. It is unknown whether hyponatremia or low osmolar condition plays roles in the pathogenesis of VC.Human vascular smooth muscle cells (VSMCs) were cultured with calcifying medium, which was supplemented high calcium and phosphate. Concentrations of sodium in the culture media were further modified to determine the impacts of osmotic pressure on VC. Microarray analysis of VSMCs revealed low osmolality activated Rac1-Akt pathway and reduced expression of NCX1, which is calcium-sodium exchanger.Lower osmolality including hyponatremic condition promotes high-phosphate-induced VC through multiple cellular processes including Rac1-Akt pathway activation.
2023-07-25 | GSE237847 | GEO
Project description:Vascular calcification (VC) is a strong predictor of cardiovascular risk, particularly in chronic kidney disease (CKD) patients, associated with increased vascular stiffness, pulse pressure, left ventricular hypertrophy and atherosclerotic plaque burden [1]. VC is currently accepted as a highly controlled multifactorial process, where the release of extracellular vesicles (EVs) with calcification capacity plays an essential role in mediating cell-induced matrix mineralization [2]. Still, questions considering mechanisms of EVs deposition in the extracellular space, and its relationship with vesicle origin, loading, calcifying capacity and role in intercellular communication remain elusive. In this work we established a proteomic approach to characterize extracellular matrix (ECM)-deposited and cell media (CM) released EVs, from an in vitro model of VC consisting of primary vascular smooth muscle cells (VSMCs), bringing new knowledge into their specific characteristics and cargo.
2025-05-06 | PXD044045 | Pride
Project description:Vascular calcification (VC) is highly prevalent in patients with chronic kidney disease (CKD). To date, effective treatments for VC are still lacking since the underlying mechanisms remains elusive. RNA-sequencing analysis revealed that the E3 ubiquitin ligase Tripartite motif 16 (TRIM16) may be a key modulator of VC. However, it remains unclear whether TRIM16-mediated ubiquitination contributes to VC. In the present study, we used LC-MS/MS to identify the substrates of TRIM16.
2024-03-27 | PXD051036 |
Project description:Chronic kidney disease (CKD) is associated with increased cardiovascular risk, morphologically characterized by vascular calcification (VC). In CKD, high serum phosphate levels result in enhanced calcification propensity and the formation of circulating crystalline nanoaggregates (calciprotein particles, CPP2) containing calcium, phosphate and serum proteins. CPP2 can induce VC directly and this is recapitulated in vascular smooth muscle cells (VSMCs) in vitro. Under physiological conditions, vascular endothelial cells (ECs), rather than VSMCs are primarily exposed to circulating CPP2. Knowledge on the modulating effects of ECs on VC development is still in its infancy. The aim of this study was to investigate the paracrine signaling between ECs and VSMCs in CPP2-induced VC. To identify secreted soluble factors for CPP2-activated ECsthis factor, CPP2-activated ECs secretome was analyzed using mass spectrometry (LC/MS).
2023-11-30 | PXD047477 |
Project description:Chronic kidney disease (CKD) is associated with increased cardiovascular risk, morphologically characterized by vascular calcification (VC). In CKD, high serum phosphate levels result in enhanced calcification propensity and the formation of circulating crystalline nanoaggregates (calciprotein particles, CPP2) containing calcium, phosphate and serum proteins. CPP2 can induce VC directly and this is recapitulated in vascular smooth muscle cells (VSMCs) in vitro. Under physiological conditions, vascular endothelial cells (ECs), rather than VSMCs are primarily exposed to circulating CPP2. Knowledge on the modulating effects of ECs on VC development is still in its infancy. The aim of this study was to investigate the calcium and bioenergetics signaling in CPP2-induced EC, including using ECs global proteome.
2024-02-06 | PXD049245 |