Tumor endothelial marker 1 is upregulated in heart after cardiac injury and participates in cardiac remodeling

Po Sheng Chen, Wen Han Feng, Tzu Hsien Tsai, Yi Kai Hong, An Sheng Lee, Kuan Cheng Chang, Hsing Chun Chung, Yen Wen Liu, Chih Cheng Hsieh, Yi Hsian Fang, Pei Jung Yang, Chawn Yau Luo, Ping Yen Liu, Tsung Lin Cheng, Yi Heng Li

研究成果: Article同行評審

3 引文 斯高帕斯(Scopus)

摘要

Tumor endothelial marker 1 (TEM1) is a transmembrane glycoprotein that appears on mesenchymal lineage-derived cells during embryogenesis, but its expression greatly reduces after birth. Re-upregulation of TEM1 is found in tumor angiogenesis, organ fibrosis and wound healing indicating its potential role in tissue remodeling and repair. The expression level and function of TEM1 in adult heart are unknown. In explanted hearts from heart failure (HF) patients received cardiac transplantation, immunofluorescence staining showed TEM1 was expressed in cardiomyocytes (CMs) and cardiac fibroblasts. Bioinformatics analysis showed TEM1 upregulation in mouse heart after coronary ligation. Cardiac TEM1 expression was reconfirmed in mouse HF induced by coronary ligation or doxorubicin injection. TEM1 expression increased in cultured CMs stimulated with mechanical stretch, doxorubicin and hypoxia. Further studies showed recombinant TEM1 (rTEM1) was a functional protein that influenced cell behaviors of CMs. It directly activated Erk and Akt through interaction with PDGF receptor. TEM1lacZ/lacZ mice had less collagen deposition and worse cardiac function than wild type mice. These results indicate that TEM1 expression increases in the heart after cardiac injury and works as a functional protein that participates in cardiac remodeling.

原文English
文章編號10532
期刊Scientific reports
12
發行號1
DOIs
出版狀態Published - 2022 12月

All Science Journal Classification (ASJC) codes

  • 多學科

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