Open AccessTissue Transglutaminase-Mediated AT1 Receptor Sensitization Underlies Pro-inflammatory Cytokine LIGHT-Induced Hypertension
Author(s) -
Chen Liu,
Renna Luo,
Wei Wang,
Zhangzhe Peng,
Gail V.W. Johnson,
Rodney E. Kellems,
Yang Xia
Publication year - 2019
Publication title -
american journal of hypertension
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.009
H-Index - 136
eISSN - 1941-7225
pISSN - 0895-7061
DOI - 10.1093/ajh/hpz018
Subject(s) - medicine , tissue transglutaminase , inflammation , angiotensin ii receptor type 1 , endocrinology , receptor , angiotensin ii , cytokine , proinflammatory cytokine , creatinine , tumor necrosis factor alpha , sensitization , pharmacology , immunology , biochemistry , chemistry , enzyme
Although numerous recent studies have shown a strong link between inflammation and hypertension, the underlying mechanisms by which inflammatory cytokines induce hypertension remain to be fully elucidated. Hypertensive disorders are also associated with elevated pressor sensitivity. Tissue transglutaminase (TG2), a potent cross-linking enzyme, is known to be transcriptionally activated by inflammatory cytokines and stabilize angiotensin II (Ang II) receptor AT1 (AT1R) via ubiquitination-preventing posttranslational modification. Here we sought to investigate the TG2-mediated AT1R stabilization in inflammation-induced hypertension and its functional consequences with a focus on receptor abundance and Ang II responsiveness.