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Angiotensin II or Leptin induce cyclooxygenase‐2, but are mutually antagonistic in mouse aortic endothelial cells
Author(s) -
Schneider Ryan A,
Hoyt Dale G
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.a1166
Subject(s) - leptin , cyclooxygenase , endocrinology , medicine , adipokine , angiotensin ii , endothelial dysfunction , endothelium , chemistry , obesity , receptor , enzyme , biochemistry
Dietary factors and obesity contribute to vascular inflammatory responses and endothelial dysfunction. Two factors, the adipokine leptin and the vasoactive peptide angtiotensin II (ANGII), may mediate vascular effects of diet and obesity. A known mediator of many pro‐inflammatory stimuli is the cyclooxygenase‐2 (COX‐2) enzyme. Here we hypothesized that treatment of endothelial cells with leptin and/or ANGII would lead to COX‐2 induction. Mouse aortic endothelial cells (MAEC) were treated with 1 uM ANGII, 50 ng leptin/ml, or both for 1, 4, and 24 h. Protein was then extracted for western blotting with a COX‐2 specific antibody. Treatment with 1 uM ANGII caused a 2.5‐ and 2.7‐fold increase in COX‐2 levels at 1 and 4 hours respectively, which returned to baseline at 24 hours. Treatment with 50 ng leptin/ml also caused 2‐ and 2.3‐fold increases in COX‐2 levels at 1 and 4 hours, respectively. Combined treatment with 1 uM ANGII and 50 ng leptin/ml, however, caused a decrease in COX‐2 protein levels at 1, 4, and 24 hours. This unexpected reduction in COX‐2 might affect endothelial function depending on diet or obesity.