Open Access

MALAT1 promotes liver fibrosis by sponging miR‑181a and activating TLR4‑NF‑κB signaling

  • Authors:
    • Yinghui Wang
    • Qiuju Mou
    • Zixin Zhu
    • Luqiang Zhao
    • Lili Zhu
  • View Affiliations

  • Published online on: October 13, 2021     https://doi.org/10.3892/ijmm.2021.5048
  • Article Number: 215
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The aim of the present study was to investigate whether long non‑coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) could modulate activation and inflammation of hepatic stellate cell (HSCs) via regulation of a microRNA (miR)‑181a‑toll like receptor (TLR)4/nuclear factor (NF)‑κB axis, thereby contributing to the development of liver fibrosis. A total of 151 patients with liver fibrosis were recruited, and the serum levels of alanine transaminase, aspartate aminotransferase and albumin were determined. Transforming growth factor (TGF)‑β1 and LPS were used to activate and induce inflammation in the human HSC cell line LX2. MALAT1 was knocked using small interfering RNA or overexpressed, and an inhibitor and mimic of miR‑181a‑5p were used to examine the effect of MALAT1 and miR‑181a‑5p on the activation and inflammation of LX2 cells. Both MALAT1 and miR‑181a‑5p expression performed well in their ability to differentiate patients with liver fibrosis from healthy volunteers, and MALAT1 expression was associated with the severity of liver fibrosis. The expression levels of TLR4 and NF‑κB were increased after stimulation with LPS or TGF‑β1, but MALAT1 knockdown or miR‑181a‑5p mimic transfection abrogated this increase. Moreover, the TGF‑β1‑induced increase in viability, proliferation, migration, adhesion and collagen production, and the LPS‑induced inflammation of LX2 cells were all reversed after MALAT1 knockdown or transfection with miR‑181a‑5p mimic. The MALAT1/miR‑181a‑5p axis was involved in regulating collagen production and inflammation by activating TLR4/NF‑κB signaling, which may be conducive to liver fibrosis treatment in the future.

Related Articles

Journal Cover

December-2021
Volume 48 Issue 6

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
Wang Y, Mou Q, Zhu Z, Zhao L and Zhu L: MALAT1 promotes liver fibrosis by sponging miR‑181a and activating TLR4‑NF‑κB signaling. Int J Mol Med 48: 215, 2021
APA
Wang, Y., Mou, Q., Zhu, Z., Zhao, L., & Zhu, L. (2021). MALAT1 promotes liver fibrosis by sponging miR‑181a and activating TLR4‑NF‑κB signaling. International Journal of Molecular Medicine, 48, 215. https://doi.org/10.3892/ijmm.2021.5048
MLA
Wang, Y., Mou, Q., Zhu, Z., Zhao, L., Zhu, L."MALAT1 promotes liver fibrosis by sponging miR‑181a and activating TLR4‑NF‑κB signaling". International Journal of Molecular Medicine 48.6 (2021): 215.
Chicago
Wang, Y., Mou, Q., Zhu, Z., Zhao, L., Zhu, L."MALAT1 promotes liver fibrosis by sponging miR‑181a and activating TLR4‑NF‑κB signaling". International Journal of Molecular Medicine 48, no. 6 (2021): 215. https://doi.org/10.3892/ijmm.2021.5048