Cited by 18Liver physiology and pathologyMicroRNA in disease regulationLiver Disease Diagnosis and Treatment

Identification lncRNA LOC102551149/miR‐23a‐5p pathway in hepatic fibrosis

Dong, Zhiheng, Li, Sha, Si, Lengge, Ma, Ruilian, Bao, Lidao, Bo, Agula·2020·European Journal of Clinical Investigation

Abstract

Background Hepatic fibrosis is a worldwide incurable disease; due to the complex and unclear mechanism, there lack the effective therapeutic targets. However, the mechanism of miR-23a-5p underling this pathological process is largely not clear. The purpose of this study was to investigate the role of miR-23a-5p in hepatic fibrosis and HSC activation. Methods The content of miR-23a-5p in hepatic fibrosis induced by N-nitrosodimethylamine (NDMA) and HSC activation induced by platelet-derived growth factor (PDGF) was detected by qRT-PCR. H&E staining, Masson staining and Shear wave electrography (SWE) were used to detect the degree of hepatic fibrosis. Immunohistochemistry staining, qRT-PCR and Western blot detect the related markers of liver fibrosis or HSC activation, as well as the related pathway genes and proteins. Dual-luciferase reporter system verifies the interaction between miR-23a-5p with PTEN or miR-23a-5p with lncRNA LOC102551149 in HSC-T6. siRNA and miRNA mimic transfer to HSC-T6 to detect the function of lncRNA LOC102551149 and miR-23a-5p on HSC activation. Results After hepatic fibrosis and HSC activation happened, the expression of miR-23a-5p was up-regulated, whereas anti-miR-23a-5p can alleviate hepatic fibrosis and HSC activation. Further research shows miR-23a-5p can target PTEN and degrade it, causing activation of PI3K/Akt/mTOR/Snail pathway. lncRNA LOC102551149 can be used as a competition endogenous RNA (ceRNA) targeting miR-23a-5p through base pairing,…

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Crossref · 10.1111/eci.13243

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  • Following liver fibrosis and hepatic stellate cell activation, up-regulated miR-23a-5p targets PTEN for degradation, activating the PI3K/Akt/mTOR/Snail pathway.

    “Following the occurrence of liver fibrosis and the activation of hepatic stellate cells, the up-regulated expression of miR-23a-5p targets phosphatase and tensin homolog (PTEN) for degradation, thereby activating the PI3K/Akt/mTOR/Snail pathway, providing a new target for improving fibrosis [18].”

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Authors
Dong, Z., Li, S., Si, L., Ma, R., Bao, L., & Bo, A.
Affiliations
  • Inner Mongolia Medical University (CN)
  • Baotou Medical College (CN)
Corresponding author
  • Bao, Lidao
  • Bo, Agula
Venue
European Journal of Clinical Investigation
Publisher
Wiley
Published
2020-05-15
Volume
50
Issue
6
Pages
e13243-e13243
ISSN
  • 0014-2972 (ISSN-L)
  • 1365-2362
OpenAlex
W3016549002
Cited by
18
References
42
Citations by year
2026: 2 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 5
FWCI
1.76
Type
journal article
Language
en
Open access
closed
Locations
  • European Journal of Clinical Investigation (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (81550047, 81760748)
Topics
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords
liver fibrosis, miR-23a-5p, hepatic stellate cell activation, PTEN, platelet-derived growth factor, therapeutic target
MeSH terms
Animals, Cell Line, Dimethylnitrosamine, Liver Cirrhosis, Blotting, Western, Phosphatidylinositol 3-Kinases, MicroRNAs, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Rats, Hepatic Stellate Cells, Gene Knockdown Techniques, Real-Time Polymerase Chain Reaction, RNA, Long Noncoding

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