Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1023034 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26249837_1.fastq.gz | Fastqsanger.gz | |||
| SRR26249837_2.fastq.gz | Fastqsanger.gz | |||
| SRR26249838_1.fastq.gz | Fastqsanger.gz | |||
| SRR26249838_2.fastq.gz | Fastqsanger.gz | |||
| SRR26249839_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: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: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 |
Project description:Purpose: Next-generation sequencing (NGS) was performed to illustrate the genetic molecular mechanism underlying varicocele (VC) pathogenesis and Morinda officinalis polysaccharide (MOP) repair effect. Methods: The male Sprague–Dawley (SD) rats (about 6-7 weeks old and 200±10g weight) were divided into three groups: 1) control group (Control); 2) experimental varicocele group (VC); 3) 300 mg kg-1 MOP administration group (VC+MOP). The next-generation RNA sequencing were performed to identify the differentially-expressed mRNA and lncRNA in left testicular tissue between each two compared group. Results: The result show that a total of 144 mRNAs and 63 LncRNAs, 63 mRNAs and 148 LncRNAs , 173 mRNAs and 54 LncRNAs were found differentially expressed between compared group VC vs. Control, VC+MOP vs. VC, and VC+MOP vs. Control respectively. Conclusions: Our study try to offer a indication for novel diagnose marker and therapeutic method, as well as provide feasible research orientations for further study.
2021-09-08 | GSE139447 | GEO
Project description:During angiosperm male gametogenesis, microspores divide to produce a vegetative cell (VC) and a male germline (MG), each with a distinct cell fate. How the MG cell/VC fate is determined remains largely unknown. Here, we report that the VC-targeted H3K27me3 erasure resulted in VC fate transition towards a gamete destination. Multi-omics and cytologic analysis reveal that H3K27me3 is essential for VC fate commitment and contributes to suppress the MG cell fate initiation in VC, whereas MG cells require H3K27me3 reprograming for the gamete cell fate. This work suggests that the MG cell/VC fate is epigenetically regulated. The dimorphic H3K27 methylation acts as a core switch to determine their distinct cell fates and ensure the functional specification of both VC and MG for pollen fertility. This work also provides direct evidences for the proposal that VC maintains the default developmental program of microspore, whereas MG requires reprogramming.
2022-08-03 | GSE162638 | GEO
Project description:During angiosperm male gametogenesis, microspores divide to produce a vegetative cell (VC) and a male germline (MG), each with a distinct cell fate. How the MG cell/VC fate is determined remains largely unknown. Here, we report that the VC-targeted H3K27me3 erasure resulted in VC fate transition towards a gamete destination. Multi-omics and cytologic analysis reveal that H3K27me3 is essential for VC fate commitment and contributes to suppress the MG cell fate initiation in VC, whereas MG cells require H3K27me3 reprograming for the gamete cell fate. This work suggests that the MG cell/VC fate is epigenetically regulated. The dimorphic H3K27 methylation acts as a core switch to determine their distinct cell fates and ensure the functional specification of both VC and MG for pollen fertility. This work also provides direct evidences for the proposal that VC maintains the default developmental program of microspore, whereas MG requires reprogramming.
2022-08-03 | GSE162637 | GEO
Project description:We examined the transcriptional profile of human kidney biopsies, aiming to provide insight into the mechanisms of progressive CKD. This approach led to the identification of FERM domain protein 3, (FRMD3) as a molecular driver of disease. Transcriptome profiling was performed in human renal biopsy tissue and correlated with parameters of kidney function, including estimated glomerular filtration rate (eGFR), degree of renal tubulointerstitial fibrosis (%TIF), as well as CKD progression over a median follow-up period of 60 months. Transcriptome analysis performed in two independent cohorts of patients with CKD (n=24 and n=17, respectively) identified a cluster of genes (n=93) significantly correlated (FDR P<0.05) with eGFR and %TIF, and associated with CKD progression, with enrichment for pathways associated with inflammation and immune-cell mediated infiltration. Expression of FRMD3, a previously reported candidate gene from human genetics studies in CKD, was negatively correlated with indices of CKD severity and progression. Knockdown of FRMD3 in human kidney epithelial cells enhanced fibrotic responses to the cytokine transforming growth factor-beta (TGF-β1). Analysis of FRMD3 binding partners indicated enrichment of proteins implicated in mitochondrial function and remodeling of epithelial adherens junctions. Lentivirus-mediated knockdown of FRMD3 in renal tubule epithelial cells yielded a significant reduction (>35%) in NAD(P)H-dependent oxidoreductase activity, and a corresponding increase in caspase activity (50%). Using global transcriptome profiling we define a cluster of transcripts associated with severity of CKD and identify loss of FRMD3 expression as a potential molecular driver. Loss of FRMD3 expression may contribute to mitochondrial function and TIF.
2024-11-06 | PXD015297 | Pride
Project description:Adenovirus-mediated FENDRR transfer to the lungs of mice reduced asbestos-induced fibrotic lesions and collagen deposition.RNA sequencing analysis was used to profile the gene expression in the lungs of asbestos-treated (VC-Cro) mice compared to control (VC-TiO2).
2021-05-26 | GSE175496 | GEO