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Loss of Interleukin-21 Receptor Activation in Hypoxic Endothelial Cells Impairs Perfusion Recovery After Hindlimb Ischemia
Author(s) -
Tao Wang,
Alexis Cunningham,
Ayotunde O. Dokun,
Surovi Hazarika,
Kevin Houston,
Lingdan Chen,
R. John Lye,
Rosanne Spolski,
Warren J. Leonard,
Brian H. Annex
Publication year - 2015
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.115.305476
Subject(s) - downregulation and upregulation , hindlimb , biology , microbiology and biotechnology , receptor , umbilical vein , in vivo , stat protein , immunology , endocrinology , medicine , apoptosis , in vitro , stat3 , biochemistry , gene
Surgical hindlimb ischemia (HLI) in mice has become a valuable preclinical model to study peripheral arterial disease. We previously identified that the different phenotypic outcomes after HLI across inbred mouse strains is related to a region on the short arm of mouse chromosome 7. The gene coding the interleukin-21 receptor (IL-21R) lies at the peak of association in this region.

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