Open Access

Laminin α5 modulates fibroblast proliferation in epidural fibrosis through the PI3K/AKT/mTOR signaling pathway

  • Authors:
    • Pengran Liu
    • Hui Chen
    • Lianqi Yan
    • Yu Sun
  • View Affiliations

  • Published online on: January 28, 2020     https://doi.org/10.3892/mmr.2020.10967
  • Pages: 1491-1500
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Lumbar laminectomy is commonly deemed as the most valid surgery for a series of lumbar illnesses, such as lumbar disc herniation, which could lead to spinal canal stenosis. However, epidural fibrosis is one of the most common complications that limits the application of lumbar laminectomy, which is mainly caused by proliferation of local fibroblasts. Laminins are glycoproteins that consist of α, β and γ chains, which serve a crucial role in biological cell behaviors, such as adhesion, differentiation, migration and proliferation, especially the isoform with the fifth α chain‑laminin α5. The PI3K/AKT/mTOR signaling pathway was demonstrated to be associated with various biological functions in cells. The aim of the present study was to explore whether laminin α5 is an important factor in epidural fibrosis by modulating the proliferation of fibroblasts through the activation of PI3K/AKT/mTOR signaling pathway. In the animal model, the results of the hematoxylin‑eosin staining, cell counting, Masson's trichrome staining and immunohistochemical staining showed laminin α5 to be positively associated with epidural fibrosis. Furthermore, to verify the assumption that laminin α5 could modulate fibroblast proliferation through the PI3K/AKT/mTOR signal pathway, fibroblasts were transfected with laminin α5‑small interfering (si)RNA. The results of western blotting (proliferating cell nuclear antigen and cyclin D1), the Cell Counting Kit‑8 and EdU incorporation assays indicated that the proliferative level of fibroblasts decreased, and the expression of phosphorylated (p)‑focal adhesion kinase 1, p‑AKT and p‑mTOR was reduced. Subsequently, laminin α5 was overexpressed and the change in cell proliferation and expression of associated proteins contrasted with that observed in siRNA. The results demonstrated that laminin α5 could interfere the activation of the PI3K/AKT/mTOR signaling pathway. Finally, the inhibition of the PI3K/AKT/mTOR signaling pathway by LY294002 resulted in decreased fibroblast proliferation. In conclusion, laminin α5 could modulate fibroblast proliferation in epidural fibrosis through the PI3K/AKT/mTOR signaling pathway.
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March 2020
Volume 21 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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APA
Liu, P., Chen, H., Yan, L., & Sun, Y. (2020). Laminin α5 modulates fibroblast proliferation in epidural fibrosis through the PI3K/AKT/mTOR signaling pathway. Molecular Medicine Reports, 21, 1491-1500. https://doi.org/10.3892/mmr.2020.10967
MLA
Liu, P., Chen, H., Yan, L., Sun, Y."Laminin α5 modulates fibroblast proliferation in epidural fibrosis through the PI3K/AKT/mTOR signaling pathway". Molecular Medicine Reports 21.3 (2020): 1491-1500.
Chicago
Liu, P., Chen, H., Yan, L., Sun, Y."Laminin α5 modulates fibroblast proliferation in epidural fibrosis through the PI3K/AKT/mTOR signaling pathway". Molecular Medicine Reports 21, no. 3 (2020): 1491-1500. https://doi.org/10.3892/mmr.2020.10967