MicroRNA-21 promotes the progression of peritoneal fibrosis through the activation of the TGF-?/Smad signaling pathway: An in vitro and in vivo study

Retraction in: /10.3892/ijmm.2020.4510

  • Authors:
    • Ya-Li Ma
    • Fang Chen
    • Su-Xia Yang
    • Bao-Ping Chen
    • Jun Shi
  • View Affiliations

  • Published online on: November 17, 2017     https://doi.org/10.3892/ijmm.2017.3268
  • Pages: 1030-1038
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The present study aimed to explore the roles of microRNA-21 (miR‑21) and the transforming growth factor-β (TGF-β)/Smad signaling pathway in the development of peritoneal fibrosis (PF). First, dialysis effluents from 30 patients with PF were collected, and after the establishment of a mouse model of PF, hematoxylin and eosin (H&E) and Masson's staining were used to observe peritoneal tissues, inflammatory cells and blood vessels. High glucose was used to stimulate human peritoneal mesothelial cell lines and these stimulated cells were then transfected with miR‑21 inhibitor. Immunofluorescence microscopy was applied for the observation of the transfected cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR‑21, and RT-qPCR and western blot analysis were used to detect the mRNA and protein expression of Zonula occludens-1 (ZO-1), TGF-β, Smad, vimentin and connective-tissue growth factor (CTGF). The mRNA and protein expression levels TGF-β, Smad-3, vimentin and CTGF were elevated, while ZO-1 mRNA and protein expression was decreased with the prolonged duration of dialysis treatment in the patients with PF. The experiments using the mouse model of PF revealed that the peritoneal connective tissue was thickened, while the numbers of inflammatory cells and blood vessels were increased. The expression levels of miR‑21, and the mRNA and protein expression levels of TGF-β, Smad-3, vimentin and CTGF were increased over time, whereas the mRNA and protein expression levels ZO-1 constantly decreased in the mice in the experimental group. Moreoever, the expression of miR‑21 positively correlated with the expression levels of TGF-β, Smad-3, vimentin and CTGF, while it negatively correlated with the expression of ZO-1. The results of H&E and Masson's staining revealed that miR‑21 expression was associated with the degree of PF. These findings thus indicate that miR‑21 promotes the progression of PF through the activation of the TGF-β/Smad signaling pathway.
View Figures
View References

Related Articles

Journal Cover

February-2018
Volume 41 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Ma Y, Chen F, Yang S, Chen B and Shi J: MicroRNA-21 promotes the progression of peritoneal fibrosis through the activation of the TGF-?/Smad signaling pathway: An in vitro and in vivo study Retraction in /10.3892/ijmm.2020.4510. Int J Mol Med 41: 1030-1038, 2018
APA
Ma, Y., Chen, F., Yang, S., Chen, B., & Shi, J. (2018). MicroRNA-21 promotes the progression of peritoneal fibrosis through the activation of the TGF-?/Smad signaling pathway: An in vitro and in vivo study Retraction in /10.3892/ijmm.2020.4510. International Journal of Molecular Medicine, 41, 1030-1038. https://doi.org/10.3892/ijmm.2017.3268
MLA
Ma, Y., Chen, F., Yang, S., Chen, B., Shi, J."MicroRNA-21 promotes the progression of peritoneal fibrosis through the activation of the TGF-?/Smad signaling pathway: An in vitro and in vivo study Retraction in /10.3892/ijmm.2020.4510". International Journal of Molecular Medicine 41.2 (2018): 1030-1038.
Chicago
Ma, Y., Chen, F., Yang, S., Chen, B., Shi, J."MicroRNA-21 promotes the progression of peritoneal fibrosis through the activation of the TGF-?/Smad signaling pathway: An in vitro and in vivo study Retraction in /10.3892/ijmm.2020.4510". International Journal of Molecular Medicine 41, no. 2 (2018): 1030-1038. https://doi.org/10.3892/ijmm.2017.3268