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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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Identification of specifically activated angiogenic molecules in HMGB-1-induced angiogenesis

  • Kim, Won Kyu (Department of Pathology and Brain Korea 21 PLUS Projects for Medical Science, Yonsei University College of Medicine) ;
  • Kwon, Yujin (Department of Pathology and Brain Korea 21 PLUS Projects for Medical Science, Yonsei University College of Medicine) ;
  • Park, Minhee (Department of Pathology and Brain Korea 21 PLUS Projects for Medical Science, Yonsei University College of Medicine) ;
  • Yun, Seongju (Department of Pathology and Brain Korea 21 PLUS Projects for Medical Science, Yonsei University College of Medicine) ;
  • Kwon, Ja-Young (Departments of Obstetrics and Gynecology, Institute of Women's Life Medical Science, Yonsei University College of Medicine) ;
  • Kim, Hoguen (Department of Pathology and Brain Korea 21 PLUS Projects for Medical Science, Yonsei University College of Medicine)
  • Received : 2017.07.12
  • Accepted : 2017.09.29
  • Published : 2017.11.30
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Abstract

High-mobility group box-1 (HMGB-1) is expressed in almost all cells, and its dysregulated expression correlates with inflammatory diseases, ischemia, and cancer. Some of these conditions accompany HMGB-1-mediated abnormal angiogenesis. Thus far, the mechanism of HMGB-1-induced angiogenesis remains largely unknown. In this study, we performed time-dependent DNA microarray analysis of endothelial cells (ECs) after HMGB-1 or VEGF treatment. The pathway analysis of each gene set upregulated by HMGB-1 or VEGF showed that most HMGB-1-induced angiogenic pathways were also activated by VEGF, although the activation time and gene sets belonging to the pathways differed. In addition, HMGB-1 upregulated some VEGFR signaling-related angiogenic factors including EGR1 and, importantly, novel angiogenic factors, such as ABL2, CEACAM1, KIT, and VIPR1, which are reported to independently promote angiogenesis under physiological and pathological conditions. Our findings suggest that HMGB-1 independently induces angiogenesis by activating HMGB-1-specific angiogenic factors and also functions as an accelerator for VEGF-mediated conventional angiogenesis.

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References

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