Interleukin-6–Signal Transducer and Activator of Transcription-3 Signaling Mediates Aortic Dissections Induced by Angiotensin II via the T-Helper Lymphocyte 17–Interleukin 17 Axis in C57BL/6 Mice
Author(s) -
Xiaoxi Ju,
Talha Ijaz,
Hong Sun,
Sutapa Ray,
Wanda S. LeJeune,
Chang Lee,
Adrián Recinos,
Dong-Chuan Guo,
Dianna M. Milewicz,
Ronald G. Tilton,
Allan R. Brasier
Publication year - 2013
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.301049
Subject(s) - angiotensin ii , stat protein , signal transduction , immunology , medicine , interleukin , interleukin 4 , endocrinology , biology , cytokine , microbiology and biotechnology , receptor , stat3
Dysregulated angiotensin II (Ang II) signaling induces local vascular interleukin-6 (IL-6) secretion, producing leukocyte infiltration and life-threatening aortic dissections. Precise mechanisms by which IL-6 signaling induces leukocyte recruitment remain unknown. T-helper 17 lymphocytes (Th17) have been implicated in vascular pathology, but their role in the development of aortic dissections is poorly understood. Here, we tested the relationship of IL-6-signal transducer and activator of transcription-3 signaling with Th17-induced inflammation in the formation of Ang II-induced dissections in C57BL/6 mice.
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