ArticleBMC nephrology2025
MiR-503-5p mediates cell cycle arrest and fibrosis of peritoneal mesothelial cells with a high peritoneal solute transport status.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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8 authors.
Funding
Abstract
backgroundLong-term peritoneal dialysis (PD) induces persistent inflammation and fibrosis of the peritoneal membrane (PM), altering the peritoneal solute transport rate (PSTR). We previously found elevated miR-503-5p levels in exosomes from PD effluent (PDE) in patients with high PSTR. As PSTR is strongly influenced by intraperitoneal inflammation, this study aimed to explore the relationship between miR-503-5p, inflammation, and peritoneal fibrosis and the underlying mechanisms.
methodsBioinformatics analyses were initially performed to identify the miR-503-5p target genes and determine the research subject. Real-time polymerase chain reaction (RT-PCR), miRNA RT-PCR, and western blotting were used to detect the expression levels of miR-503-5p and its targets in human MeT-5A mesothelial cells. A cell counting kit-8 assay was used to ascertain the impact of miR-503-5p on cellular proliferation, and cell cycle was evaluated using a FACScan flow cytometer. The miR-503-5p target genes were identified using mimic/inhibitor transfection and dual-luciferase reporter assays. The PDE exosomes (PDE-exos) labeled with PKH67 were used to observe their interactions with MeT-5A cells.
resultsPatients with PD who exhibited an increasing PSTR had notably elevated dialysate interleukin (IL)-6 concentrations, which demonstrated a positive correlation with the PSTR. The induction of lipopolysaccharides remarkably enhanced the expression of miR-503-5p and IL-6 in peritoneal mesothelial cells (PMCs). Overexpression of miR-503-5p induced cell cycle arrest in the G1/S phase and notably upregulated the expression of fibrotic indicators (alpha-smooth muscle actin and type I collagen) in PMCs. Cyclin D1 was a direct target of miR-503-5p and expressed in PMCs. Additionally, PKH67-labeled PDE-exos were internalized by PMCs.
conclusionsPatients with PD who had a high PSTR exhibited an elevated inflammatory state, and the presence of inflammatory factors stimulated the upregulation of miR-503-5p expression, which led to cell cycle arrest in PMCs and promoted peritoneal fibrosis development.
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