Tumor Endothelial Marker 1 (TEM1/Endosialin/CD248) Enhances Wound Healing by Interacting with Platelet-Derived Growth Factor Receptors

Yi Kai Hong, Yao Chou Lee, Tsung Lin Cheng, Chao Han Lai, Chao Kai Hsu, Cheng Hsiang Kuo, Yun Yan Hsu, Jui Ting Li, Bi Ing Chang, Chih Yuan Ma, Shu Wha Lin, Kuan Chieh Wang, Guey Yueh Shi, Hua Lin Wu

Research output: Contribution to journalArticle

Abstract

Tumor endothelial marker 1 (TEM1), also known as endosialin or CD248, is a type I transmembrane glycoprotein containing a C-type lectin-like domain. It is highly expressed in pericytes and fibroblasts. Dermal fibroblasts play a pivotal role during cutaneous wound healing, especially in the proliferative phase. However, the physiological function of TEM1 in wound healing is still undetermined. During the process of wound healing, the expression of both TEM1 and platelet-derived growth factor (PDGF) receptor α was highly upregulated in myofibroblasts. In vivo, fibroblast activation and collagen deposition in granulation tissues were attenuated, and wound healing was retarded in TEM1-deleted mice. In vitro, the migration, adhesion, and proliferation of NIH3T3 cells were suppressed following TEM1 knockdown by short hairpin RNA. In PDGF-BB–treated NIH3T3 cells, the downstream signal and mitogenic, and chemoattractive effects were inhibited by TEM1 knockdown. In addition, TEM1 and PDGF receptor α were colocalized in subcellular organelles in fibroblasts, and the association of TEM1 and PDGF receptor α was demonstrated by coimmunoprecipitation. In summary, these findings suggested that TEM1, in combination with PDGF receptor α, plays a critical role in wound healing by enhancing the mitogenic and chemoattractive effects of PDGF-BB and collagen deposition in myofibroblasts.

Original languageEnglish
Pages (from-to)2204-2214.e7
JournalJournal of Investigative Dermatology
Volume139
Issue number10
DOIs
Publication statusPublished - 2019 Oct

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Platelet-Derived Growth Factor Receptors
Tumor Biomarkers
Wound Healing
Tumors
Fibroblasts
Myofibroblasts
Collagen
C-Type Lectins
Pericytes
Skin
Granulation Tissue
Platelet-Derived Growth Factor
Granulation
Organelles
Small Interfering RNA
Glycoproteins
Cell Proliferation
Adhesion
Chemical activation
Association reactions

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

Hong, Yi Kai ; Lee, Yao Chou ; Cheng, Tsung Lin ; Lai, Chao Han ; Hsu, Chao Kai ; Kuo, Cheng Hsiang ; Hsu, Yun Yan ; Li, Jui Ting ; Chang, Bi Ing ; Ma, Chih Yuan ; Lin, Shu Wha ; Wang, Kuan Chieh ; Shi, Guey Yueh ; Wu, Hua Lin. / Tumor Endothelial Marker 1 (TEM1/Endosialin/CD248) Enhances Wound Healing by Interacting with Platelet-Derived Growth Factor Receptors. In: Journal of Investigative Dermatology. 2019 ; Vol. 139, No. 10. pp. 2204-2214.e7.
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abstract = "Tumor endothelial marker 1 (TEM1), also known as endosialin or CD248, is a type I transmembrane glycoprotein containing a C-type lectin-like domain. It is highly expressed in pericytes and fibroblasts. Dermal fibroblasts play a pivotal role during cutaneous wound healing, especially in the proliferative phase. However, the physiological function of TEM1 in wound healing is still undetermined. During the process of wound healing, the expression of both TEM1 and platelet-derived growth factor (PDGF) receptor α was highly upregulated in myofibroblasts. In vivo, fibroblast activation and collagen deposition in granulation tissues were attenuated, and wound healing was retarded in TEM1-deleted mice. In vitro, the migration, adhesion, and proliferation of NIH3T3 cells were suppressed following TEM1 knockdown by short hairpin RNA. In PDGF-BB–treated NIH3T3 cells, the downstream signal and mitogenic, and chemoattractive effects were inhibited by TEM1 knockdown. In addition, TEM1 and PDGF receptor α were colocalized in subcellular organelles in fibroblasts, and the association of TEM1 and PDGF receptor α was demonstrated by coimmunoprecipitation. In summary, these findings suggested that TEM1, in combination with PDGF receptor α, plays a critical role in wound healing by enhancing the mitogenic and chemoattractive effects of PDGF-BB and collagen deposition in myofibroblasts.",
author = "Hong, {Yi Kai} and Lee, {Yao Chou} and Cheng, {Tsung Lin} and Lai, {Chao Han} and Hsu, {Chao Kai} and Kuo, {Cheng Hsiang} and Hsu, {Yun Yan} and Li, {Jui Ting} and Chang, {Bi Ing} and Ma, {Chih Yuan} and Lin, {Shu Wha} and Wang, {Kuan Chieh} and Shi, {Guey Yueh} and Wu, {Hua Lin}",
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Tumor Endothelial Marker 1 (TEM1/Endosialin/CD248) Enhances Wound Healing by Interacting with Platelet-Derived Growth Factor Receptors. / Hong, Yi Kai; Lee, Yao Chou; Cheng, Tsung Lin; Lai, Chao Han; Hsu, Chao Kai; Kuo, Cheng Hsiang; Hsu, Yun Yan; Li, Jui Ting; Chang, Bi Ing; Ma, Chih Yuan; Lin, Shu Wha; Wang, Kuan Chieh; Shi, Guey Yueh; Wu, Hua Lin.

In: Journal of Investigative Dermatology, Vol. 139, No. 10, 10.2019, p. 2204-2214.e7.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Tumor Endothelial Marker 1 (TEM1/Endosialin/CD248) Enhances Wound Healing by Interacting with Platelet-Derived Growth Factor Receptors

AU - Hong, Yi Kai

AU - Lee, Yao Chou

AU - Cheng, Tsung Lin

AU - Lai, Chao Han

AU - Hsu, Chao Kai

AU - Kuo, Cheng Hsiang

AU - Hsu, Yun Yan

AU - Li, Jui Ting

AU - Chang, Bi Ing

AU - Ma, Chih Yuan

AU - Lin, Shu Wha

AU - Wang, Kuan Chieh

AU - Shi, Guey Yueh

AU - Wu, Hua Lin

PY - 2019/10

Y1 - 2019/10

N2 - Tumor endothelial marker 1 (TEM1), also known as endosialin or CD248, is a type I transmembrane glycoprotein containing a C-type lectin-like domain. It is highly expressed in pericytes and fibroblasts. Dermal fibroblasts play a pivotal role during cutaneous wound healing, especially in the proliferative phase. However, the physiological function of TEM1 in wound healing is still undetermined. During the process of wound healing, the expression of both TEM1 and platelet-derived growth factor (PDGF) receptor α was highly upregulated in myofibroblasts. In vivo, fibroblast activation and collagen deposition in granulation tissues were attenuated, and wound healing was retarded in TEM1-deleted mice. In vitro, the migration, adhesion, and proliferation of NIH3T3 cells were suppressed following TEM1 knockdown by short hairpin RNA. In PDGF-BB–treated NIH3T3 cells, the downstream signal and mitogenic, and chemoattractive effects were inhibited by TEM1 knockdown. In addition, TEM1 and PDGF receptor α were colocalized in subcellular organelles in fibroblasts, and the association of TEM1 and PDGF receptor α was demonstrated by coimmunoprecipitation. In summary, these findings suggested that TEM1, in combination with PDGF receptor α, plays a critical role in wound healing by enhancing the mitogenic and chemoattractive effects of PDGF-BB and collagen deposition in myofibroblasts.

AB - Tumor endothelial marker 1 (TEM1), also known as endosialin or CD248, is a type I transmembrane glycoprotein containing a C-type lectin-like domain. It is highly expressed in pericytes and fibroblasts. Dermal fibroblasts play a pivotal role during cutaneous wound healing, especially in the proliferative phase. However, the physiological function of TEM1 in wound healing is still undetermined. During the process of wound healing, the expression of both TEM1 and platelet-derived growth factor (PDGF) receptor α was highly upregulated in myofibroblasts. In vivo, fibroblast activation and collagen deposition in granulation tissues were attenuated, and wound healing was retarded in TEM1-deleted mice. In vitro, the migration, adhesion, and proliferation of NIH3T3 cells were suppressed following TEM1 knockdown by short hairpin RNA. In PDGF-BB–treated NIH3T3 cells, the downstream signal and mitogenic, and chemoattractive effects were inhibited by TEM1 knockdown. In addition, TEM1 and PDGF receptor α were colocalized in subcellular organelles in fibroblasts, and the association of TEM1 and PDGF receptor α was demonstrated by coimmunoprecipitation. In summary, these findings suggested that TEM1, in combination with PDGF receptor α, plays a critical role in wound healing by enhancing the mitogenic and chemoattractive effects of PDGF-BB and collagen deposition in myofibroblasts.

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