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. 2021 Feb 20;11(9):4207–4231. doi: 10.7150/thno.48530

Figure 5.

Figure 5

KLK (kallikrein-related peptidase) 8 deficiency attenuates diabetic endothelial damage and endothelial-to-mesenchymal transition. Plasma samples and heart tissues were obtained from the KLK8-deficient (KLK8-/-) and KLK8+/+ mice after 24 weeks of diabetes. A-C, Plasma levels of thrombomodulin (A), von Willebrand factor (B) and E-selectin (C). D & E, Immunoblots of VE-cadherin, CD31, vimentin and α-SMA in the hearts. The representative protein bands (D) and the corresponding histograms (E) showed that the loss of CD31 and VE-cadherin in diabetic heart tissues was largely prevented, whereas the acquisition of α-SMA and vimentin was dramatically decreased in KLK-/- mice. F & G, Immunofluorescent staining showed decreased colocalization of α-SMA (F, green), FSP-1 (G, green) and CD31 (red) in the hearts obtained from KLK8-/- diabetic mice as compared to KLK8+/+ diabetic mice. Nuclei were counterstained with DAPI (blue), scale bar = 50 µm. Data are expressed as means ± SEM (n = 7). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.