Tumor Endothelial Marker 1 (TEM1/endosialin/CD248) Enhances Wound Healing Process by Cooperation with Platelet‐Derived Growth Factor (PDGF) Receptor

Abstract

Tumor endothelial marker 1 (TEM1), also named endosialin and CD248, is a type I transmembrane glycoprotein containing a C‐type lectin‐like domain. TEM1 is highly expressed on tumor‐associated fibroblasts, stromal cells, pericytes, and dermal fibroblasts. Dermal fibroblasts play a pivotal role in cutaneous wound healing which occurs in three dynamic and overlapping but distinct stages, including inflammatory phase, proliferation phase, and remodeling phase. However, the physiological function of TEM1 in wound healing is still unknown. In wound healing process both TEM1 and platelet‐derived growth factor receptor α (PDGFRα) expressions were highly upregulated in myofibroblasts. The cell activation, proliferation, and collagen deposition in granulation tissues were decreased and slower wound healing was found in TEM1‐deleted mice. In addition, the cell migration, adhesion and proliferation in NIH3T3 cells were decreased when TEM1 expression was knockdown by shRNA. The downstream signaling, mitogenic, and chemoattractive effects of platelet‐derived growth factor‐BB‐treated NIH3T3 cells were inhibited by knockdown of TEM1. TEM1 and PDGFRα were co‐localized in sub‐cellular organelles in fibroblasts and could be co‐immunoprecepitated. Based on these results we proposed that TEM1 in combination with PDGFRα plays a critical role in wound healing by enhancing the mitogenic and chemoattractive effects of platelet‐derived growth factor‐BB and collagen deposition in myofibroblasts.Support or Funding InformationThis work was supported by a grant from the Ministry of Science and Technology, Executive Yuan, Taiwan. (MOST 105‐2320‐B‐006 ‐039 ‐MY3 to Hua‐Lin Wu)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.