Excessive proliferation and migration of fibroblasts in the lumbar
laminectomy area can lead to epidural
fibrosis, eventually resulting in
failed back surgery syndrome. It has been reported that
laminin α1, a significant biofunctional
glycoprotein in the extracellular matrix, is involved in several fibrosis‑related diseases, such as pulmonary, liver and
keloid fibrosis. However, the underlying mechanism of
laminin α1 in epidural
fibrosis remains unknown. The present study aimed to explore the effect and mechanism of
laminin α1 in fibroblast proliferation, apoptosis and migration, and epidural
fibrosis. Following the establishment of a
laminectomy model,
hematoxylin and
eosin, Masson's trichrome and immunohistochemical staining were performed to determine the degree of epidural
fibrosis, the number of fibroblasts,
collagen content and the epidural expression levels of
laminin α1, respectively. Furthermore, a stable
small interfering RNA system was used to knock down the expression of
laminin α1 in fibroblasts. The transfection efficiency was confirmed by reverse transcription‑quantitative PCR and immunofluorescence staining. Western blot analysis, scratch
wound assay, EdU incorporation assay, flow cytometric analysis and Cell Counting Kit 8 assay were performed to assess the proliferation, apoptosis, migration and viability of fibroblasts, as well as the expression levels of the AKT/mechanistic target of
rapamycin (mTOR) signaling‑related
proteins. In vivo experiments revealed that
laminin α1 was positively and time‑dependently associated with epidural
fibrosis. In addition,
laminin α1 knockdown attenuated cell proliferation, viability and migration, and promoted apoptosis. Furthermore, the results revealed that the activation of the AKT/mTOR signaling pathway was involved in the aforementioned processes. Overall, the current study illustrated the positive association between
laminin α1 and epidural
fibrosis, and also verified the effect of
laminin α1 on fibroblast proliferation, apoptosis and migration. Furthermore, the results suggested that the AKT/mTOR signaling pathway may serve a significant role in regulating the behavior of
laminin α1‑induced fibroblasts.