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T cells mediate angiotensin II‐induced aortic stiffening
Author(s) -
Wu Jing,
Thabet Salim R.,
Kirabo Annet,
Trott Daniel W.,
Goldstein Anna,
Hudson Billy G,
Madhur Meena S.,
Chen Wei,
Harrison David G.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.906.7
Subject(s) - angiotensin ii , adventitia , medicine , chemistry , endocrinology , elastin , renin–angiotensin system , angiotensin ii receptor type 1 , receptor , pathology , blood pressure
In this study, we sought to determine if T cells mediate aortic stiffening in hypertension. Histological studies showed that chronic angiotensin II infusion caused profound collagen deposition in the aortic adventitia of wild‐type (WT), but not lymphocyte deficient (RAG‐1−/−) mice. Biochemical analysis confirmed that angiotensin II increased collagen from 3.3±0.02 to 6.6±0.5 μg/mm (sham vs ang II, p<0.01, n=5) in WT mice but not in Rag‐1−/− mice. Total elastin was neither different between mouse strains nor changed by angiotensin II. Angiotensin II decreased aortic compliance (measured in isolated pressured vessels) in WT mice by 60% (p<0.01, n=8), but not in Rag‐1−/− mice. Adoptive transfer of pan T cells into Rag‐1−/− mice restored the aortic stiffening and collagen deposition caused by angiotensin II. Studies with interferon gamma (IFN‐γ) and IL‐17A deficient mice indicated that both of these cytokines contribute to aortic collagen deposition and stiffening. In conclusion, T cells are essential for angiotensin II‐induced collagen deposition and aortic stiffening. Part of these effects are mediated by T cell‐derived cytokines such as IFN‐γ and IL‐17A.