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Inhibition of VSMC Activation and Vascular Restenosis by Interleukin‐19
Author(s) -
Ellison Stephen,
Richards James,
Miecyjak Alex,
Gabunia Khatuna,
Kelemen Sheri,
Autieri Michael
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.870.2
Subject(s) - neointima , vascular smooth muscle , restenosis , endocrinology , medicine , ligation , stimulation , interleukin , cytokine , chemistry , smooth muscle , stent
This study tested the hypothesis that IL‐19, a member of the Th2 family of anti‐inflammatory interleukins, can attenuate vascular restenosis and modulate the vascular smooth muscle cell (VSMC) response to injury. Carotid artery ligation of hyper‐responsive wild‐type (wt) mice (FVB strain) injected with 10ng/g/day rIL‐19 had significantly lower neointima/media ratio (N/I) compared with PBS controls (P=0.006). Conversely, carotid artery of IL‐19 knock out (KO) mice demonstrated significantly higher N/I ratio compared with wt mice (both non‐responding C57B/6 strain) (P=0.04). Importantly, the increased N/I ratio in the KO could be rescued by injection of 10ng/g/day into the KO mouse (P=0.04). VSMC explanted from IL‐19 KO mice proliferated significantly more rapidly compared with wt (P=0.04). Addition of IL‐19 to cultured wt VSMC did not significantly decrease VSMC proliferation, but could rescue KO VSMC to wild‐type levels (P=0.02). KO VSMC expressed significantly greater levels of inflammatory mRNA including IL‐1β, TNFα, and MCP‐1 in response to TNFα stimulation (P<0.01 for all). No polarization of adaptive immunity was noted in these mice. Together, these data indicate that IL‐19 is a previously unrecognized anti‐inflammatory factor for VSMC, and plays an important protective role in vascular restenosis.