Basic Research

Tumor endothelial markers1 mediate endothelial cell angiogenesis and heart failure myocardial remodeling via MAPKs pathway

  • Ting XU ,
  • Wei HUANG ,
  • Li YANG ,
  • Hao. YU
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  • Department of Cardiology,Wuhan First Hospital (Wuhan Hospital of Integrated Traditional Chinese and Western Medicine),Wuhan 430022,China

Received date: 2023-07-04

  Online published: 2024-04-08

Abstract

Objective To explore the role of endothelial cells in angiogenesis and myocardial remodeling in heart failure based on MAPKs pathway mediated by tumor endothelial marker 1 (TEM1). Methods Sixty-four mice were equally randomized into four groups: sham operation, myocardial infarction (MI), MI+sh-NC and MI+sh-TEM1. On the 7th day after MI, the changes of EndMT in the infarct border area were detected by immunofluorescence staining, and the cardiac function of mice was evaluated by echocardiography on the 28th day. Mouse aortic endothelial cells (MAECs) were divided into three groups: control, Vector and rTEM1. In addition, MAECs were pretreated with MAPK inhibitor SB203580, and the cells were treated with rTEM1 for 48 h. The changes of EndMT and MAPKs signaling pathways in endothelial cells were evaluated by Western blot. Results In the myocardium at the border of infarction, the level of TEM1-1 increased slightly on the 1st day after MI, reached the peak on the 7th day, and then decreased on the 28th day. Compared with Vector group, the expression of VE-Cadherin protein in the rTEM1 group decreased significantly (P < 0.05), and the levels of α-SMA and vimentin, relative migration distance, the number of invading cells, and the number of branching formation increased significantly (P < 0.05). SB203580 reversed these changes of MAECs induced by rTEM1. Compared with the MI group, the co-staining level of CD31+Vimentin+ in the MI+sh-TEM1 group decreased significantly (P < 0.01). On the 28th day, the LVEF and LVFS in the MI+sh-TEM1 group were significantly higher than those in MI group (P < 0.05). Compared with the MI group, the expressions of p-P38/P38 and p-JNK/JNK in the endothelial cells of the MI+sh-TEM1 group decreased. Conclusion EndMT and angiogenesis induced by TEM1 participate in the pathogenesis of cardiac fibroblasts induced by MI, which may be mechanically related to the activation of MAPKs signaling pathway.

Cite this article

Ting XU , Wei HUANG , Li YANG , Hao. YU . Tumor endothelial markers1 mediate endothelial cell angiogenesis and heart failure myocardial remodeling via MAPKs pathway[J]. The Journal of Practical Medicine, 2024 , 40(6) : 780 -786 . DOI: 10.3969/j.issn.1006-5725.2024.06.009

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