2011 Fiscal Year Final Research Report

Macrophage differentiation in abdominal aortic aneurysm via IL-6 signals

Research Project

Project/Area Number	22791264
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	General surgery
Research Institution	Kurume University
Principal Investigator	OHNO Satoko 久留米大学, 医学部, 助教 (80569418)
Project Period (FY)	2010 – 2011
Keywords	血管外科学 / 大動脈瘤 / サイトカイン
Research Abstract	In this project, we investigated the hypothesis that IL-6/JAK/STAT pathway is activated and involved in the pathogenesis of abdominal aortic aneurysm(AAA), using human AAA tissue culture and mouse model of AAA. We found that human AAA tissue secrets large amount of IL-6 in culture media, and JAK/STAT pathway is involved in the secretion of a subset of inflammatory cytokines. We also found that JAK/STAT pathway is activated in mouse model of AAA during the rapid expansion of the diameter. However, macrophage-specific deletion of SOCS3 gene(mSOCS3-KO), which should enhance the IL-6 signal, did not affect the formation of AAA in mice. Unexpectedly, mSOCS3-KO showed greater susceptibility to acute aortic dissection(AAD) upon the angiotensin II infusion compared to wild type mice. Thus, macrophage IL-6 signal appears to be dispensable for AAA development, but essential to AAD development in mouse models.

(4 results)