The mechanism of anti-cardiac fibrosis effect of TAX1BP1 on mice diabetic cardiomyopathy model

Objective To investigate the mechanism of TAX1BP1 on cardiac fibrosis in mice model of DCM. Methods Mice were subjected to STZ injection to induce type 1 DCM model. 12 weeks after final injection, mice were subjected to myocardial injection of advurus-TAX1BP1 to overexpress TAX1BP1. At 16 weeks after final STZ injection, hearts were removed. Immunohistochemical staining was used to assess CD31, α-SMA expression level. Immunofluorescence staining was used to assess vascular endothelial (VE)-cadherin, collagen Ⅲ expression. Western blot was used to detect VE-cadherin, CD31, α-SMA, and vimentin expression level in each group. Results The microvascular density assessed by CD31 staining was significantly decreased in the model group, while increased in the TAX1BP1 overexpression model group (P<0.05). The expression of α-SMA in the model group was higher than that in the control group, which was decreased in TAX1BP1 overexpression-model group (P<0.05). Double fluorescence labeling result showed that compared with the control group, the expression of VE-cadherin was decreased and collagen Ⅲ was increased in the model group (P<0.05). These was changed by TAX1BP1 overexpression. Western blot showed that the expression of VE-cadherin and CD31 were decreased, α-SMA and vimentin were increased in the model group. These was also changed by TAX1BP1 overexpression (P<0.05). Conclusion TAX1BP1 may suppress the development of cardiac fibrosis in the diabetic process by inhibiting endothelin mesenchymal transformation. Key words: Diabetic cardiomyopathies; Fibrosis; Endothelial cells