Fig 2: Loss of PRDX2 exacerbates inflammation in aneurysmal lesions.Analysis of abdominal aortas from Prdx2+/+ and Prdx2-/- mice infused with saline or Ang II for 4 weeks. a Immunoblotting analysis of ICAM-1, VCAM-1, CD45, and PRDX2 in aortas from Prdx2+/+ and Prdx2-/- mice infused with saline or Ang II for 4 weeks. ß-actin was used as a loading control. b Quantification of ICAM-1, c VCAM-1, and d CD45 in Fig. 6a. Data are presented as the mean ± SEM (two-tailed Student’s t test). e Representative immunostaining images showing the accumulation of immune cells in aneurysmal lesions. Cross-sectional images of CD45 immunostaining (top; scale bar, 200 µm) and higher magnification of the boxed area (bottom; scale bar, 100 µm). f Quantification of CD45-positive cells using images of abdominal aortic cross-sections (saline groups, n = 3; Ang II groups, n = 5). Data are presented as the mean ± SEM (two-tailed Student’s t test). g Representative confocal images of immune cells (CD45) and macrophages (MOMA2) in aneurysmal aortas. Scale bar, 50 µm. h The levels of IL-1ß and i IL-6 in plasma from Prdx2+/+ and Prdx2-/- mice infused with saline or Ang II for 4 weeks. Data are presented as the mean ± SEM (two-tailed Student’s t test).

Fig 3: Identification of L-plastin and PRDXs in K562 cells. Conditioned media (CM) was collected and TCA precipitated, and the protein was extracted from cell lysates (CL) of K562 and MDA-MB-231 cells (MD-231). a) Intracellular and released L-plastin, PRDX2 and PRDX4 in K562 and MDA-MB-231 cells were assessed by immunoblotting. b) K562 cells were cultured at different cell densities (105–106 cells/ml) and the levels of L-plastin, PRDX2 and PRDX4 in CM were assessed by immunoblotting. Ponceau stain (lower gels) was used as loading control. Shown are representative immunoblots from one out five independent experiments.

Fig 4: The Kaplan-Meier method was used to calculate the DFS and OS between the group of patients with high PRDX2 expression and the group of patients with low PRDX2 expression, and the log-rank test was used to analyze the difference between groups. It was revealed that among HCC patients, high expression of PRDX2 was associated with longer (A) OS (P<0.001) and (B) DFS (P<0.001), while low PRDX2 expression revealed shorter (A) OS (P<0.001) and (B) DFS (P<0.001). OS, overall survival; DFS, disease-free survival; PRDX2, peroxiredoxin2; HCC, hepatocellular carcinoma.

Fig 5: Antler chondrocytes can highly express a variety of peroxiredoxins, and the expression of PRDX2 upregulates as the chondrocytes mature. (A) The expression level of PRDX family protein by qRT-PCR in antler chondrocytes. (B) The expression level Col2a (chondrocyte marker molecule) by qRT-PCR in antler pre-chondrocytes (PCC) and chondrocytes (CC). (C) The expression level of PRDX1-6 by qRT-PCR in PCC and CC. (D) Immunohistochemistry staining of PRDX2 in the antler pre-cartilage layer and cartilage layer. (a) Negative control, (b) pre-cartilage layer, (c) cartilage layer. Scale bar, 50 µm. The data include the means ± SD of three independent experiments. ** p < 0.01, *** p < 0.001.