Abstract
MiRNAs contribute greatly to epithelial to mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs), which is a crucial step in peritoneal fibrosis (PF). In this study, we tried to profile whether miRNA expression differences exist after human umbilical cord mesenchymal stem cells (hUCMSCs) treatment in PF rats and investigate the possible role of miR‐153‐3p involved in anti‐EMT process. We randomly assigned 34 rats into three groups: control group (Group Control), MGO‐induced PF rats (Group MGO) and hUCMSCs‐treated rats (Group MGO + hUCMSCs). MiRNA microarrays and real‐time PCR analyses were conducted in three groups. α‐SMA, Snail1 and E‐cadherin expression were detected by Western blot. Luciferase reporter assays were used to detect the effects of miR‐153‐3p overexpression on Snai1 in rat peritoneal mesothelial cells (RPMCs). We identified differentially expressed miRNAs related to EMT, in which miR‐153‐3p demonstrated the greatest increase in Group MGO + hUCMSCs. Transient cotransfection of miR‐153‐3p mimics with luciferase expression plasmids resulted in a significant repression of Snai1 3′‐untranslated region luciferase activity in RPMCs. These studies suggest that miR‐153‐3p is a critical molecule in anti‐EMT effects of hUCMSCs in MGO‐induced PF rats. MiR‐153‐3p might exert its beneficial effect through directly targeting Snai1.
Highlights
Chronic kidney disease (CKD) represents a common health problem worldwide, and their prevalence continues to increase.[1]
In Rat peritoneal mesothelial cells (RPMCs). (ii) miRNAs related to epithelial to mesenchymal transition (EMT) are differentially expressed in the MGO-induced peritoneal tissues of rats after human umbilical cord mesenchymal stem cells (hUCMSCs) treatment. (iii) miR-153-3p showed the greatest increase in the MGO-induced peritoneal tissues of rats after hUCMSCs treatment contributed to anti-EMT effects by directly targeting Snai[1]
It has been proposed that collagen type I/III ratio is an important marker of ECM overexpression and accumulation.15The current data indicate that Mesenchymal stem cells (MSCs) represent a promising candidate in direct antifibrotic treatment of various fibrotic diseases.[16,17]
Summary
Chronic kidney disease (CKD) represents a common health problem worldwide, and their prevalence continues to increase.[1]. Patients with CKD were usually occult and, so far, lack of early diagnosis and treatment methods, which is eventually led to end-stage renal disease (ESRD). Peritoneal fibrosis (PF), which is lack of effective prevention and control countermeasures, is one of the most important factors that force patients with ESRD to interrupt from longterm PD, restricts the application and development of PD.[4]. Despite this potential, the mechanisms and signalling pathways involved in hUCMSCs-mediated PF repair are poorly understood. We tested the protective effects of hUCMSCs treatment on methylglyoxal (MGO)-induced PF in rats and tried to profile whether differences existed in peritoneal miRNA expression of control rats, MGO-induced PF rats and hUCMSCs-treated rats. We hypothesized that the greatest increased miR-153 is overlapped among the three groups contributed to the attenuation of MGOinduced PF in rats
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