Mechanisms of Epithelial-Mesenchymal Transition of Peritoneal Mesothelial Cells During Peritoneal Dialysis

Epithelial-mesenchymal transition (EMT) plays an important role in peritoneal metastasis of Gastric cancer (GC). Tumor exosomes can mediate tumor directed metastasis, and TGF-β1 is an important factor in inducing tumor Epithelial mesenchymal transition. However, it is not clear whether GC derived exosomes can induce peritoneal mesothelial cells through the TGF-β1/ Smads pathway and the effect of injured peritoneal mesothelial cells on the biological characteristics of GC cells. In this study, we demonstrated that GC-derived exosomes can activate the TGF-β1/Smads pathway in peritoneal mesothelial cells and induce the corresponding EMT process, and that the injured peritoneal mesothelial cells can improve the migration and adhesion of GC cells. Taken together, these data further support the critical role of exosomes in the remodeling of the pre-metastatic microenvironment.

Download Full-text

Effect of lactate as a peritoneal dialysis fluid buffer on rat peritoneal mesothelial cells

Renal Replacement Therapy ◽

10.1186/s41100-020-00306-8 ◽

2020 ◽

Vol 6 (1) ◽

Author(s):

Chieko Higuchi ◽

Junko Kuriyama ◽

Hiroshi Sakura

Keyword(s):

Peritoneal Dialysis ◽

Growth Factor ◽

Mesothelial Cells ◽

Matrix Metalloproteinase 2 ◽

Dialysis Fluid ◽

Mesenchymal Transition ◽

Peritoneal Mesothelial Cells ◽

Peritoneal Dialysis Fluid ◽

E Cadherin

Abstract Background Neutral, low-glucose degradation product (GDP) peritoneal dialysis fluid (PDF) is less damaging to the peritoneum than conventional PDF but is still insufficient for biocompatibility. One remaining issue is the problem of buffering. Methods Using cultured rat peritoneal mesothelial cells (PMCs), the present study examined the difference between the effects of neutral low-GDP lactate PDF and neutral low-GDP bicarbonate/lactate PDF on cells. The effects of lactate stimulation on these cells were also examined. Results Lactate PDF enhanced mRNA expressions of α-smooth muscle actin (αSMA) and type 1 and type 3 collagens and lowered expression of e-cadherin mRNA in PMCs compared to bicarbonate/lactate PDF. Lactate stimulation increased mRNA expressions of αSMA, matrix metalloproteinase 2 (MMP2), and basic fibroblast growth factor (bFGF) and suppressed e-cadherin mRNA expression. Transforming growth factor (TGF)-β1 and TGF-β2 and collagen type 1 and 3 mRNA expressions were also enhanced by lactate stimulation. Conclusions These results suggest that lactate as a PDF buffer may act on PMCs to promote epithelial-mesenchymal transition (EMT) and production of TGF-β, bFGF, and collagen.

Download Full-text

The Effect of Statin on Epithelial-Mesenchymal Transition in Peritoneal Mesothelial Cells

PLoS ONE ◽

10.1371/journal.pone.0109628 ◽

2014 ◽

Vol 9 (10) ◽

pp. e109628 ◽

Cited By ~ 16

Author(s):

Tae Ik Chang ◽

Hye-Young Kang ◽

Kyung Sik Kim ◽

Sun Ha Lee ◽

Bo Young Nam ◽

...

Keyword(s):

Epithelial Mesenchymal Transition ◽

Mesothelial Cells ◽

Mesenchymal Transition ◽

Peritoneal Mesothelial Cells

Download Full-text

MiR-30b is involved in methylglyoxal-induced epithelial-mesenchymal transition of peritoneal mesothelial cells in rats

Cellular & Molecular Biology Letters ◽

10.2478/s11658-014-0199-z ◽

2014 ◽

Vol 19 (2) ◽

Cited By ~ 19

Author(s):

Hong Liu ◽

Ning Zhang ◽

Da Tian

Keyword(s):

Mirna Expression ◽

Epithelial Mesenchymal Transition ◽

Degradation Products ◽

Mesothelial Cells ◽

Control Group ◽

Peritoneal Fibrosis ◽

Expression Array ◽

Mesenchymal Transition ◽

Peritoneal Mesothelial Cells

AbstractEpithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMC) is a major contributor to the pathogenesis of peritoneal fibrosis. EMT is at least in part caused by repeated exposure to glucose degradation products (GDPs), such as methylglyoxal (MGO). MiRNA contributes greatly to the EMT of PMCs. In this study, we tried to profile whether differences exist between the peritoneal membrane (PM) miRNA expression seen in control rats and that seen in rats injected intraperitoneally with MGO. We assessed whether miR-30b has a possible role in MGO-induced EMT of PMCs in rats. Comparative miRNA expression array and real-time PCR analyses were conducted for the control group at the start of the experiment and for the MGO group after 1 and 2 weeks. During the second week, the MGO rats were treated with: a chemically modified antisense RNA oligonucleotide (ASO) complementary to the mature miR-30b (ASO group); an miR-30b mismatch control sequence (MIS group); or a citrate buffer (EMT group). Bioinformatic analyses indicated that the 3′ untranslated region (3′-UTR) of bone morphogenetic protein 7 (BMP7) mRNA did contain a putative binding site for miR-30b. We also tried to investigate whether miR-30b targeted BMP7 in vitro by transfection. Of the upregulated miRNAs, miR-30b expression demonstrated the greatest increase. The administration of miR-30b ASO for two weeks significantly reduced α-SMA excretion and upregulated E-cadherin and BMP-7 expression. Our in vitro study showed that miR-30b directly targeted and inhibited BMP7 by binding to its 3’-UTR. Our results revealed that miR-30b is involved in MGO-induced EMT of PMCs in rats.

Download Full-text