Premium
Synergistic co‐operation of signal transducer and activator of transcription 5B with activator protein 1 in angiotensin II‐induced angiotensinogen gene activation in vascular smooth muscle cells
Author(s) -
Han Mei,
Li AiYing,
Meng Fang,
Dong LiHua,
Zheng Bin,
Hu HaiJuan,
Nie Lei,
Wen JinKun
Publication year - 2009
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2009.06902.x
Subject(s) - angiotensin ii , activator (genetics) , vascular smooth muscle , renin–angiotensin system , medicine , stat protein , endocrinology , chemistry , immediate early gene , stimulation , gene expression , messenger rna , angiotensin receptor , gene , biology , microbiology and biotechnology , phosphorylation , stat3 , smooth muscle , biochemistry , blood pressure
The binding sequences for signal transducer and activator of transcription (STAT) and activator protein 1 have been found in the promoter region of the angiotensinogen gene. We examined whether the elements for activator protein 1 and STAT5B function in angiotensinogen gene activation induced by angiotensin II in vascular smooth muscle cells. Stimulation with angiotensin II increased the level of angiotensinogen mRNA by 2.1‐fold in vascular smooth muscle cells. The increased level of angiotensinogen mRNA occurred with concurrent elevations in the levels of STAT5B and c‐Jun phosphorylation after stimulation with angiotensin II. Likewise, angiotensin II resulted in similar enhancements of the DNA‐binding activity of STAT5B and c‐Jun in angiotensin II‐induced angiotensinogen expression. Notably, the STAT5B–DNA complex interacted with the c‐Jun–DNA complex by forming a stable quaternary complex in angiotensin II‐induced angiotensinogen expression. Our findings support a model in which co‐operative interaction of STAT5B and activator protein 1 bound to the the promoter region provides maximal activation of angiotensinogen expression by angiotensin II in vascular smooth muscle cells.