Journal
FRONTIERS IN GENETICS
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fgene.2020.599834
Keywords
traumatic brain injury; vasculature; endothelial cell; IGFBP7; TGF beta
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Funding
- National Natural Science Foundation of China [81870978, 81702489, 81911530166, 82002659]
- National Key R&D Program of China [2018YFC1313003]
- Tianjin Natural Science Foundation [18JCYBJC94000]
- Natural Science Foundation of Shaanxi Province [2020JQ-429]
- Fundamental Research Funds for the Central University [GK202003050, GK202003048]
- Natural Science Foundation of Huaihua City [2020R3118, 2020R3116]
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The study reveals key molecular alterations in endothelial cells in response to TBI, including increased Myc targets and Epithelial-Mesenchymal Transition signatures; IGFBP7 is identified as a potential biomarker for vascular response to TBI; TGF beta signaling may contribute to the upregulation of IGFBP7 in the vasculature.
Vasculature plays critical roles in the pathogenesis and neurological repair of traumatic brain injury (TBI). However, how vascular endothelial cells respond to TBI at the molecular level has not been systematically reviewed. Here, by integrating three transcriptome datasets including whole cortex of mouse brain, FACS-sorted mouse brain endothelial cells, and single cell sequencing of mouse brain hippocampus, we revealed the key molecular alteration of endothelial cells characterized by increased Myc targets and Epithelial-Mesenchymal Transition signatures. In addition, immunofluorescence staining of patients' samples confirmed that IGFBP7 was up-regulated in vasculature in response to TBI. TGF beta 1, mainly derived from microglia and endothelial cells, sufficiently induces IGFBP7 expression in cultured endothelial cells, and is significantly upregulated in response to TBI. Our results identified IGFBP7 as a potential biomarker of vasculature in response to TBI, and indicate that TGF beta signaling may contribute to the upregulation of IGFBP7 in the vasculature.
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