Premium
Angiotensin II induces AT1 receptor upregulation by oxidative stress and activation of AP1 and NF‐κB in two neuronal cell lines
Author(s) -
Liu Dongmei,
Gao Lie,
Roy Shyamal K.,
Zucker Irving H.
Publication year - 2007
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.21.6.a889-d
Subject(s) - ap 1 transcription factor , downregulation and upregulation , angiotensin ii , angiotensin ii receptor type 1 , c jun , oxidative stress , chemistry , receptor , transcription factor , apocynin , junb , activator (genetics) , medicine , endocrinology , microbiology and biotechnology , biology , nadph oxidase , biochemistry , gene
In a previous study, we showed Angiotensin II (Ang II) upregulated Ang II type I receptors (AT1R) in the rostral ventrolateral medulla of normal and heart failure rabbits. The present study investigated if oxidative stress plays a role in Ang II induced AT1R upregulation, its relationship to the transcription factors activator protein 1 (AP1) and nuclear factor‐ κB (NF‐κB) in CATHa and NG 108 neuronal cell lines. Data are presented in the table. In the CATHa cell line, Ang II increased AT1R mRNA by 2.5 fold versus untreated cells; Tempol and Apocynin reversed the increased AT1R expression. Ang II also increased c‐Jun mRNA by 2.0 fold. Inhibitors of AP1 (Tanshinone IIA) and NF‐κB (6‐Amino‐4‐quinazoline) blocked the Ang II induced AT1R and c‐Jun transcription. We also examined these responses in the NG 108 neuronal cell line. Ang II increased AT1 mRNA by 3.1 fold versus untreated cells. Tempol, Apocynin, AP1 and NF‐κB inhibitors all reversed the increased AT1R transcription in response to Ang II. These data suggest that Ang II induces AT1R upregulation at the transcriptional level by activation of AP1 and NF‐κB in CATHa and NG‐108 cell lines. Oxidative stress may be one route for Ang II to elicit AP1 and NF‐κB related genes transcription. Supported by NIH grant PO‐1 HL 62222