Vimentin-Rab7a Pathway Mediates the Migration of MSCs and Lead to Therapeutic Effects on ARDS

Figure 2

Vimentin knockout alleviated the therapeutic effect of MSCs on ARDS. Two hours after inducing ARDS in mice, MSCs from wild-type mice and vimentin knockout mice were injected, and the mice were housed for 1 W, 4 W, and 16 W. Lung tissue was stained by H&E (a) and quantified by calculating alveolar thickness (b). Masson staining (c, d) and α-SMA immunohistochemical staining (e, f) were performed on the 16 W lung tissue to assess the degree of pulmonary fibrosis. On the second day after LPS induction of ARDS, the alveolar lavage fluid of each group of mice was collected, labelled with CD11c and F4/80, and then counted via flow cytometry (g) to clarify the differentiation of MSCs. In order to observe the effect of MSCs on the release of ARDS inflammatory factors, the peripheral serum of mice was collected at 1 D, 3 D, 5 D, 1 W, 2 W, 4 W, 8 W, and 16 W after LPS-induced ARDS, and TNF-α (h), TGF-β (i), and INF-γ (j) contents were tested. Two hours after the ARDS model was constructed, MSCs from GFP-labeled wild-type mice and vimentin knockout mice were injected through the tail vein of the mouse. At 24 h, 48 h, 72 h, and 96 h, the left lung tissue of the mouse was obtained and observed under a British crown microscope. GFP-labelled cells (k). Statistical results are represented by . , , .

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