Similar Datasets
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:To investigate the distribution of H3.3B in VSMC phenotypic transition, we infect VSMCs with shNT or shH3f3b virus.
2024-04-06 | GSE229127 | GEO
Project description:We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in VSMC dedifferentiation. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PJ34,and mRNA sequence were performed. We found that PDGF-BB could upregualted the genes involved in cell proliferation and migration, and downregulated the VSMC contractile genes, all of which could be reversed by PARP inhibitor PJ34. Then we knockdowned the co-factor Myocardin in VSMCs, and found the above effects of PJ34 were nearly abolished.Our study first provided the transcription changes by RNA-seq in VSMC dedifferentiation, and demonstrated the key roles of PARP1 and the PARylation process in VSMC phenotypic switch.
2018-09-20 | GSE103995 | GEO
Project description:Atherosclerosis is one of the causative factors leading to the development of cardiovascular disease. Angiotensin II (AngII) is implicated in the pathological processes underlying atherosclerosis. We investigated the AngII regulated gene expression in primary vascular smooth muscle cells (VSMC). VSMCs were isolated from the thoracic aorta of male Wistar rats. Serum deprived VSMCs were stimulated with 100 nM AngII or vehicle for 2 hours, then RNA-Sequencing was carried out.
2022-07-03 | E-MTAB-11863 | biostudies-arrayexpress
Project description:Conduit arterial disease in CKD is an important cause of cardiac complications. Cardiac function in CKD has not been studied in the absence of arterial disease. In an Alport syndrome model bred not to have conduit arterial disease, mice at 225 days of life (dol) had CKD equivalent to human stage 4-5 CKD. PTH and FGF23 levels were one log order elevated, circulating sclerostin was elevated, and renal activin A was strongly induced. Aortic Ca levels were not increased and VSMC transdifferentiation was absent. The CKD mice were not hypertensive, and cardiac hypertrophy was absent. Freshly excised cardiac tissue respirometry (Oroboros) showed ADP-stimulated O2 flux was diminished from 52 to 22 pmol/mg (p=0.022). RNAseq of cardiac tissue from CKD mice revealed significantly decreased levels of cardiac mitochondrial oxidative phosphorylation genes. The data reported here show that cardiac mitochondrial respiration is impaired in CKD in the absence of conduit arterial disease. This is the first report of the direct effect of CKD on cardiac respiration.
2024-02-23 | GSE255815 | GEO
Project description:Vascular smooth muscle cells (VSMCs) are a major cell type of the arterial wall and their functionality is associated with blood pressure regulation. Although royal jelly (RJ) has reported effects on anti-hypertension, the mechanism of blood pressure regulation by major royal jelly protein 1 (MRJP1), the most abundant RJ protein, is still unknown. Therefore, mrjp1 gene was delivered into mouse VSMCs to investigate how MRJP1 influences the VSMC functionality by functional and proteomic analysis.The data here are the proteomic analysis of triplicated control and MRJP1 expressing VSMCs.
2018-10-27 | PXD004207 | Pride
Project description:Vascular calcification is a complex process and has been associated with aging, diabetes, chronic kidney disease (CKD). Although there have been several studies studying the role of miRNAs (miRs) in bone osteogenesis, little is known about the role of miRs in vascular calcification and their role in the pathogenesis of vascular abnormalities. Matrix vesicles (MV) are known to play an important role in initiating vascular smooth muscle cell (VSMC) calcification. In the present study, we performed miRNA microarray analysis to identify the dysregulated miRs between MV and VSMC derived from CKD rats to understand the role of post-transcriptional regulatory networks governed by these miRNAs in vascular calcification and to uncover the differential miRNA content of MV. The percentage of miRNA to total RNA was increased in MV compared to VSMC. Comparison of expression profiles of miRNA by microarray demonstrated 33 miRs to be differentially expressed with the majority (~ 57%) of them down-regulated. Target genes controlled by differentially expressed miRNAs were identified utilizing two different complementary computational approaches Miranda and Targetscan to understand the functions and pathways that may be affected due to the production of MV from calcifying VSMC thereby contributing to the regulation of genes by miRs. We found several processes including vascular smooth muscle contraction, response to hypoxia and regulation of muscle cell differentiation to be enriched. Signaling pathways identified included MAP-kinase and wnt signaling that have previously been shown to be important in vascular calcification. In conclusion, our results demonstrate that miRs are concentrated in MV from calcifying VSMC, and that important functions and pathways are affected by the miRs dysregulation between calcifying VSMC and the MV they produce. This suggests that miRs may play a very important regulatory role in vascular calcification in CKD by controlling an extensive network of post-transcriptional targets. Compare miRNA from matrix vesicles to miRNA from vascular smooth muscle cells that gave rise to the matrix vesicles from 3 sets of MV and VSMC derived from 3 normal and 3 CKD rats
2015-06-12 | E-GEOD-68913 | biostudies-arrayexpress
Project description:HIF1α is a key regulator of hypoxia, however, the changes of its target genes in VSMCs under hypoxia were unknown. CoCl2 is a chemical hypoxia agent which leads to the stabilization of HIF1-α and the expression of hypoxia responsive genes, Therefore Hif1afl/fl and Hif1a△SMC VSMCs were treated with CoCl2 and performed microarray analysis. We used microarray to detail the gene expression of WT (Hif1afl/fl) mice and VSMC-specific HIF1α disruption (Hif1a△SMC) mice VSMCs treated with 150μM CoCl2 for 24hours.
2020-06-22 | GSE119226 | GEO
Project description:Patients with chronic kidney disease (CKD) are at markedly increased risk of disability, hospitalization, and death. Impaired physical function, which is common in CKD, is a major risk factor for these poor outcomes. CKD patients perform substantially below age-predicted norms on a variety of clinically relevant physical performance tests. Altered muscle physiology is an important cause of these functional deficits. We recently described skeletal muscle fibrosis in the vastus lateralis muscle of patients with severely impaired kidney function. Greater severity of fibrosis was associated with lower leg extension strength and reduced endurance capacity, suggesting that muscle fibrosis in CKD patients is functionally significant. An important unanswered question is whether muscle fibrosis in CKD is a slowly progressive process beginning with early loss of kidney function, or a complication observed only with severe disease. Here, we examined the associations of estimated glomerular filtration rate (a measure of kidney function) with measures of fibrosis across a broad range of kidney function, and tested the effect of receiving treatment with dialysis. We also integrated muscle transcriptomic analyses to provide further insight into this novel aspect of muscle pathology in CKD.
2021-03-01 | GSE157712 | GEO
Project description:Purpous: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathway. The goals of this study are to compare different gene expression between pAd-KLF5- and pAd-Control-infected mouse VSMC. Methods: adenovirus vectors either encoding KLF5 or empty adenovirus vector were transfected into mouse VSMCs. shSirt6 transfected or shControl transfected VSMCs samples were performed RNA sequencing (RNA-seq) analysis, functional enrichment analyses of gene ontology (GO) and gene set enrichment analysis (GSEA). Results: eIF5a is found to be highly expressed and predictive target of KLF5 in VSMCs. KLF5-enhanced VSMCs demonstrated cell proliferation and were noted to have promoted cell cycle progression between the G2 and M phases. In accordance with the gene set enrichment analysis (GSEA) according to RNA-sequencing, ATP biosynthesis and cell redox homeostasis was upregulated upon KLF5 overexpression. Conclusion: These findings provide mechanistic insights into the oncogenic activity of KLF5 for the first time.
2020-09-09 | GSE148765 | GEO