Molecular mechanisms for suppressing the migration of endothelial cells by excessive VEGF

2019 Fiscal Year Final Research Report

• Project/Area Number: 19K21231
• Project/Area Number (Other): 18H06113 (2018)
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund (2019); Single-year Grants (2018)
• Review Section: 0801:Pharmaceutical sciences and related fields
• Research Institution: Kitasato University
• Principal Investigator: Akane Morita 北里大学, 薬学部, 助教 (00828072)
• Project Period (FY): 2018-08-24 – 2020-03-31
• Keywords: 血管内皮細胞 / 血管生物学

Outline of Final Research Achievements

This study aimed to investigate the molecular mechanisms of the phenomenon that excessive VEGF suppresses the migration of vascular endothelial cells in neonatal mouse retina. We found that higher concentrations of VEGF attenuated the migratory response of human umbilical vein endothelial cells, without decreasing the cell viability, proliferative activity, and level of phosphorylation of VEGF receptor 2. These results suggest that optimal concentration range of VEGF enhances both migration and proliferation of the endothelial cells, leading to the proper direction of angiogenesis.

Free Research Field

医歯薬学

Academic Significance and Societal Importance of the Research Achievements

強力な血管新生促進因子として知られている VEGF が、血管内皮細胞の遊走を至適な濃度では促進するものの、高濃度になると抑制に転じさせることを見出した本研究は、これまでの血管新生における VEGF の概念を覆す基礎生物医学的に意義深い成果をもたらしたとともに、血管新生が問題となる眼疾患の病態解明や様々な虚血性疾患の治療に対しても応用可能な概念を生み出した。