Fig 1: The TCA cycle pathway was inactivated in primary AT2 cells of septic-ALI mice. (a) Screening for differentially expressed genes in the peripheral blood of healthy donors (N = 34) and septic-ALI patients (N = 30). (b) KEGG analysis of 3918 downregulated genes and 1372 upregulated genes. (c, d) Expression of ACLY, ACO1, CS, DLAT, DLST, FH, IDH1, IDH3A, MDH1, MDH2, PDHA1,PDHB, SDHA, SUCLA2, and SUCLG2 was detected in the (c) GSE32707 dataset, or in septic-ALI mice (N = 10) and control mice (N = 10) via RT-PCR detection in (d) AT2 cells. (e, f) Expression of MDH1 and MDH2 was done via (e) WB assay (N = 5) and (f) immunofluorescence assay in AT2 cells (N = 5). *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 2: MDH1 or MDH2 promoted the proliferation and invasion of primary AT2 cells by promoting glucose uptake. (a, b) RT-PCR and (c, d) WB were used to detect the effect of siRNA and overexpressed plasmid on AT2 cells. (e) MDH1 or MDH2 promoted the glucose uptake of AT2 cells. (f) The proliferation of AT2 cells was dependent on glucose. (g, h) The effect of MDH1 or MDH2 on the proliferation of AT2 cells was measured in (g) 100% high-glucose medium or (h) 100% glucose-free medium via CCK-8. (i) The effect of MDH1 or MDH2 on the proliferation of AT2 cells was measured via EdU assays in 100% high-glucose medium. (j) The invasion of AT2 cells was dependent on glucose. (k, l) The effect of MDH1 or MDH2 on the invasion of AT2 cells was measured in 100% high-glucose medium (k) or 100% glucose-free medium (l) via transwell assay. *P < 0.05, **P < 0.01, ***P < 0.001; NS: no significance.
Fig 3: MDH1 or MDH2 inhibited the apoptosis of primary AT2 cells by promoting glucose uptake. (a) The apoptosis ratio of primary AT2 cells was detected in PBS- or LPS-treated mice. (b) The apoptosis of AT2 cells was dependent on glucose. (c) The effect of MDH1 or MDH2 on the apoptosis of AT2 cells was measured in 100% high-glucose medium via flow cytometry. ***P < 0.001.
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