Human placental mesenchymal stem cells inhibit occurrence of pulmonary fibrosis by regulating transforming growth factor-beta 1/Smad3 signaling pathway

doi:10.12307/2024.712

Abstract

Abstract: BACKGROUND: Human placental mesenchymal stem cells have been shown to be effective in inhibiting the development of pulmonary fibrosis, but the underlying mechanisms remain unclear.
OBJECTIVE: To investigate the therapeutic effect and related mechanism of human placental mesenchymal stem cells on silica-induced pulmonary fibrosis in human embryonic lung fibroblasts (MRC-5).
METHODS: CCK-8 assay was used to detect the effects of different mass concentrations of silica on the proliferation of MRC-5 at different time points. Immunofluorescence staining was used to screen out the best stimulating mass concentration and time of silica for subsequent experiments. MRC-5 cells were divided into blank group, silica group, and silica + human placental mesenchymal stem cell group. In the blank group, cells were not treated. In the silica group, MRC-5 cells were stimulated with 100 μg/mL silica for 48 hours. In the silica + human placental mesenchymal stem cell group, MRC-5 cells were stimulated with 100 μg/mL silica for 48 hours and then co-cultured with human placental mesenchymal stem cells for 24 hours. Immunofluorescence staining was used to detect the expression of α-smooth muscle actin and collagen type I in cells of each group. Western blot assay was used to detect the expressions of pulmonary fibrosis-related proteins and TGF-β1/Smad 3 signaling pathway-related proteins in cells of each group.
RESULTS AND CONCLUSION: (1) CCK-8 assay results suggested that 100 μg/mL silica was the best mass concentration and time to stimulate MRC-5 cells for 48 hours. (2) Immunofluorescence staining results showed that the expression of α-smooth muscle actin and collagen type I in the silica + human placental mesenchymal stem cell group was significantly lower than that in the silica group. (3) Western blot assay results showed that compared with the silica group, the protein expression levels of α-smooth muscle actin, collagen type I, N-cadherin, fibronectin, transforming growth factor-β1, p-Smad3, and Smad3 in the silica + human placental mesenchymal stem cell group were decreased, and the expression of E-cadherin was increased. The difference was statistically significant (P < 0.05). (4) The results showed that human placental mesenchymal stem cells had a significant therapeutic effect on silica-induced pulmonary fibrosis. Human placental mesenchymal stem cells can inhibit the development of pulmonary fibrosis by regulating transforming growth factor-β1/Smad3 signaling pathway.

Key words: human placental mesenchymal stem cell, pulmonary fibrosis, MRC-5 cell, transforming growth factor-β1, Smad3, signaling pathway

CLC Number:

Cao Jiawei, Ding Shaorui, Tie Hua, Xue Jing, Jia Yuanyuan, Liang Xueyun, Li Feng. Human placental mesenchymal stem cells inhibit occurrence of pulmonary fibrosis by regulating transforming growth factor-beta 1/Smad3 signaling pathway[J]. Chinese Journal of Tissue Engineering Research, 2024, 28(31): 4970-4974.

Figures/Tables 6

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