Molecular mechanisms involved in aquired abnormalities of tumor endothelial cells under hypoxic environment

2014 Fiscal Year Final Research Report

• Project/Area Number: 23792096
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Morphological basic dentistry
• Research Institution: Hiroshima University
• Principal Investigator: KITAYAMA Kazuko 広島大学, 医歯薬保健学研究院, 特任助教 (10515068)
• Research Collaborator: KATO Yukio 広島大学, 医歯薬保健学研究院, 研究員 ; HARA Maiko 株式会社ツーセル, 開発部, 社員
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 血管内皮細胞 / 間葉系幹細胞 / 無血清培地 / 糖脂質糖鎖

Outline of Final Research Achievements

To understand molecular mechanisms involved in acquired abnormalities of tumor vascular endothelial cells under hypoxic condition, I tried to set up a cell culture system that normal vascular endothelial cells grow malignatly in serum free STK medium, that was established for mesenchymal cells such as mesenchymal stem cells and fibroblasts, in combination with tumor cell culture conditioned medium and CoCl2. However, I failed to set up a reproducible cell culture system because of unstable cell adhesion.
On the other hand, when I cultured the mesencymal cells with medium for endothelial cells (EGM2), I found that EGM2 contained a common factor with STK that affected glycosphingolipid biosynthesis in mesenchymal cells but not in endothelial cells under responsible glycosyltransferase gene expression. These results suggested that different regulation of glycosphingolipid glycan expression is one of a reasons why endothelial cell adhesion under serum free STK medium was unstable.

Free Research Field

細胞生物学、分子生物学