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The biological mechanisms related to hub genes in the development of heart failure in dialysis patients were investigated through transcriptome sequencing

ABSTRACT: The biological mechanisms related to hub genes in the development of heart failure in dialysis patients were investigated through transcriptome sequencing

PROVIDER: PRJNA1065902 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27596746_1.fastq.gz	Fastqsanger.gz
	SRR27596746_2.fastq.gz	Fastqsanger.gz
	SRR27596747_1.fastq.gz	Fastqsanger.gz
	SRR27596747_2.fastq.gz	Fastqsanger.gz
	SRR27596748_1.fastq.gz	Fastqsanger.gz

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Project description:Chronic exposure to biological incompatibility of peritoneal dialysis solution is one of the principal causes of ultrafiltration failure (UF). However, the changes of peritoneal cell composition and molecular mechanism of peritoneal microenvironment after long-term PD are unclear. Single-cell RNA sequencing was performed to profile cell composition and transcriptome characteristics in effluent obtained from patients undergoing PD with short vintage (SV), long vintage without ultrafiltration failure (LV_NOT_UF), and long vintage with ultrafiltration failure (LV_UF). A total of 6 SV patients, 6 LV_NOT_UF patients, and 4 LV_UF patients were enrolled. The median PD duration of the three groups were 5 months (range:1.0–6.0 months), 137 months (range: 92–189 months) and 132 months (range: 120–161 months), with no significant differences in age (38.3 ± 21.5 years, 45.7 ± 10.6 years and 41.0 ± 16.7 years, P>0.05) and gender (male%: 33.3%, 50.0% and 25.0%, P>0.05). scRNA-seq data annotated 8 main cell types including epithelial-like mesothelial cells (E-MCs), mesenchymal-like mesothelial cells (M-MCs), fibroblast, plasma B cells, conventional dendritic cells, plasmacytoid dendritic cells, natural killer T cells, and myeloid cells. LV_UF patients showed higher proportion of E-MCs, which exhibited activated autophagy and had properties of both anti-inflammatory and pro-inflammatory, and neutrophil- and autophagy-related DEGs of E-MCs were upregulated in the LV_UF group. In contrast, the M-MCs and the AQP1 expression in the peritoneal mesenchyme were reduced in the LV_UF group compared to the other groups. The neutrophils in PD effluent were elevated in the LV_UF group, while the M2-like MRC1-macrophages gradually decreased from the SV, LV_NOT_UF to LV_UF group. Compared with the LV_NOT_UF group, the upregulated DEGs of monocytes/macrophages in the LV_UF group not only involved in pro-inflammatory response, but also promoted EMT progress. Additionally, neutrophils and monocytes/macrophages both interacted with MCs. Our study uncovers peritoneal different individual cell populations and cellular functions in different stages of PD which indicates the dynamic changes of microenvironments of peritoneal membrane. These findings provide new insights into the novel roles of mesothelial cells and inflammatory cells in UF.

Project description:In patients with severe kidney disease AVF are surgically placed in order to create good access for hemodialysis. In these dialysis patients the failure rates of AVF can be as high as 24% within 6 months after surgery, causing ineffective dialysis and necessitating additional clinical interventions. The pathological processes known to lead to AVF failure are beginning to be unravelled include the formation of venous neointimal hyperplasia (VNIH), thrombosis (Chang et al. PMID 16105066), and venous stenosis (Kanterman et al. PMID7892454, Tang et al. 1998), resulting in a reduced blood flow through the fistula. We established a rat model for AVF failure in human kidney dialysis patients. The characterization of this model has been previously described (Globerman et al. 2011, PubmedID:22002501). In this model the AVFs are surgically constructed in the right leg by connecting the superficial epigastric vein SEV to the common femoral artery (CFA), resulting in exposure of the SEV to arterial pressure with pulsatile and low resistant flow patterns (Globerman et al. 2011, PMID22002501). In the present study we utilized this AVF model in order to assess the effects of arterialized flow, with consequent pathological changes of the vessel wall due to surgical AVF instalment, on the transcriptome of endothelium from the SEV. Within the SEV these pathologies of the vessel wall include the formation of NIH in the main branch, and stenosis in the side branches. By employing this rat model we assessed the changes of the endothelial transcriptome in relation to these pathologies in order to gain mechanistic understanding of the potential roles of venous endothelium in AVF failure, as well as to identify potential biomarkers preceding AVF failure. AVF surgery was performed on N=6 rats, and 13-14 days after surgery the rats were sacrificed. AVFs were extracted from the rats, and microarray transcriptome analyses were performed on luminal endothelial cells that isolated from four different sites of the AVF by employing Laser Capture Microdissection (LCM). These sites included (i) N=5 AVF sections of the superficial epigastric vein (SEV) with neointimal hyperplasia (NIH), (ii) N=3 AVF sections of SEV side branches with luminal stenosis, (iii), N=6 sections of the SEV located distally from a ligation thereby omitting exposure to arterialized flow and consequently preventing the development of NIH or stenosis, and (iv) N=3 sections of the AVF common femoral artery without signs of NIH or stenosis.

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The biological mechanisms related to hub genes in the development of heart failure in dialysis patients were investigated through transcriptome sequencing

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