The elucidation of the role of chronic inflammation in heart failure.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390064
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General pharmacology
• Research Institution: Shitennoji University (2014); Osaka City University (2012-2013)
• Principal Investigator: IWAO Hiroshi 四天王寺大学, 教育学部, 教授 (00137192)
• Co-Investigator(Kenkyū-buntansha): IZUMI Yasukatsu 大阪市立大学, 大学院医学研究科, 准教授 (10347495)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: マクロファージ / エクソソーム / 心リモデリング / 内皮細胞

Outline of Final Research Achievements

Hypertension is one of the most important cardiovascular risk factors, and results in macrophage infiltration into the tissues. Here, we investigated the role of exosome, one of extracellular vesicles, in the inflammatory pathways of endothelial cells (ECs) under hypertensive conditions.
Exosomes were purified by ultracentrifugation. The exosomes isolated from angiotensin II-infused rat serum abundantly contained macrophage marker proteins, CD68 and CD45. Moreover, exosomes from hypertensive rat serum immediately activated intracellular signals such as c-jun N-terminal kinase and p38 mitogen-activated protein kinase, and upregulated the expression of intracellular adhesion molecule-1 in ECs. Interestingly, exosomes from THP-1-derived macrophages stimulated by Angiotensin II also activated these signaling pathways in ECs.
These results suggest that macrophage-derived exosomes under hypertensive conditions activate the inflammatory pathway in ECs, leading to cardiovascular remodeling.

Free Research Field

薬理学、教育学