# LncRNA RPL29P2 promotes peritoneal fibrosis and impairs peritoneal transport function via miR-1184 in peritoneal dialysis

## TL;DR

This study identifies a long noncoding RNA, RPL29P2, that contributes to peritoneal fibrosis and transport dysfunction in peritoneal dialysis patients.

## Contribution

The study discovers RPL29P2 as a novel lncRNA involved in peritoneal fibrosis and identifies miR-1184 as its target.

## Key findings

- RPL29P2 is upregulated in peritoneal membranes of long-term PD patients and correlates with fibrosis severity.
- RPL29P2 targets miR-1184 and promotes collagen expression, contributing to fibrosis and transport dysfunction.
- Silencing RPL29P2 in a rat model reduces fibrosis and prevents loss of peritoneal transport function.

## Abstract

Peritoneal dialysis (PD), hemodialysis and kidney transplantation are the three therapies to treat uremia. However, PD is discontinued for peritoneal membrane fibrosis (PMF) and loss of peritoneal transport function (PTF) due to damage from high concentrations of glucose in PD fluids (PDFs). The mechanism behind PMF is unclear, and there are no available biomarkers for the evaluation of PMF and PTF. Using microarray screening, we found that a new long noncoding RNA (lncRNA), RPL29P2, was upregulated in the PM (peritoneal membrane) of long-term PD patients, and its expression level was correlated with PMF severity and the PTF loss. In vitro and rat model assays suggested that lncRNA RPL29P2 targets miR-1184 and induces the expression of collagen type I alpha 1 chain (COL1A1). Silencing RPL29P2 in the PD rat model might suppress the HG-induced phenotypic transition of Human peritoneal mesothelial cells (HPMCs), alleviate HG-induced fibrosis and prevent the loss of PTF. Overall, our findings revealed that lncRNA RPL29P2, which targets miR-1184 and collagen, may represent a useful marker and therapeutic target of PMF in PD patients.