Fig. 4

The role and mechanism of CD90 fibroblasts in pulmonary fibrosis. Thy-1 overexpression, significant decrease in the expression of MMP-2, Occludin, α-SMA, wave proteins, and β-linked protein; and phosphorylation of β-linked protein, i.e. inactivation of the WNT pathway, thereby decreasing lung fibrosis. Thy-1 expression was associated with downregulation of the anti-apoptotic molecules Bcl-2 and Bcl-xL, and an increase in caspase-9 levels. Thy-1-pulmonary fibroblasts are resistant to apoptosis. Stimulation of lung fibroblasts with lipopolysaccharide (LPS) inhibits Thy-1 expression and upregulates integrin β3 (Itgb3) to activate the PI3K-Akt-mTOR pathway and inhibit lung fibroblast autophagy. When Thy-1 is overexpressed or integrin β3 is inhibited, LPS-induced autophagy inhibition and lung fibrosis are prevented. Thy-1-pulmonary fibroblasts secrete twice as much TGF-β as the Thy-1⁺ subset, and TGF-β1 significantly upregulates IL-1Rt1 expression in Thy-1-fibroblasts. TGF-β and interleukin-1 (IL-1) are important players in the development of pulmonary fibrosis