BDNF regulates inflammatory cytokine expressions through TrkB in human vascular endothelial cells

Research Project

Project/Area Number	25463218
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Periodontology
Research Institution	Hiroshima University
Principal Investigator	Takeda Katsuhiro 広島大学, 医歯薬保健学研究院, 助教 (10452591)
Co-Investigator(Kenkyū-buntansha)	Shiba Hideki 広島大学, 医歯薬保健学研究院(歯), 教授 (60260668)
Project Period (FY)	2013-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000) Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Keywords	脳由来神経栄養因子 / ＢＤＮＦ / 炎症性サイトカイン / ＩＣＡＭ－１ / BDNF
Outline of Final Research Achievements	Brain-derived neurotrophic factor (BDNF) enhances periodontal tissue regeneration. Tissue regeneration is characterized by inflammation which directs the quality of tissue repair. In this study, we investigated the effect of BDNF on intercellular adhesion molecule (ICAM)-1, which is an inflammatory marker, expression in interleukin (IL)-1β-treated human microvascular endothelial cells (HMVECs). We demonstrate that BDNF attenuates the IL-1β-increased ICAM-1 mRNA and protein expressions. In addition, we studied the effect of BDNF on neutrophil-like differentiated HL-60 cells adhesion to HMVECs by cell adhesion assay. Treatment of HMVECs with IL-1β led to an increase in the number of adherent neutrophil-like HL-60 cells. BDNF decreased significantly the number of neutrophil-like HL-60 cells attached HMVECs. In conclusion, BDNF may reduce excess inflammation through reduced neutrophil recruitment by regulating the ICAM-1 expression.