TY - JOUR
T1 - Induction of IkappaB: atrial natriuretic peptide as a regulator of the NF-kappaB pathway
AU - Kiemer, Alexandra K.
AU - Weber, Nina C.
AU - Vollmar, Angelika M.
PY - 2002
Y1 - 2002
N2 - Atrial natriuretic peptide (ANP) was shown to possess anti-inflammatory potential due to its potency to inhibit the production of inflammatory mediators, such as TNF-alpha. The aim of this study was to determine potential effects of ANP on endothelial cells targeted by TNF-alpha. HUVEC were treated with TNF-alpha and expression of adhesion molecules was investigated by FACS and RT-PCR. Pre-treatment of cells with ANP (30min) significantly reduced TNF-alpha-induced cell surface protein and mRNA expression of E-selectin and ICAM-1, whereas it did not influence VCAM-1. ANP reduced TNF-alpha-induced NF-kappaB activity, which was paralleled by a decreased translocation of p65 to nuclei. ANP did not alter TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, but attenuated degradation of IkappaB-epsilon. Moreover, ANP leads to a transcriptional induction of IkappaB-alpha. The induction of IkappaB by ANP is suggested as a novel mechanism for regulating inflammatory signalling in endothelial cells, leading to reduced TNF-alpha-induced expression of adhesion molecules
AB - Atrial natriuretic peptide (ANP) was shown to possess anti-inflammatory potential due to its potency to inhibit the production of inflammatory mediators, such as TNF-alpha. The aim of this study was to determine potential effects of ANP on endothelial cells targeted by TNF-alpha. HUVEC were treated with TNF-alpha and expression of adhesion molecules was investigated by FACS and RT-PCR. Pre-treatment of cells with ANP (30min) significantly reduced TNF-alpha-induced cell surface protein and mRNA expression of E-selectin and ICAM-1, whereas it did not influence VCAM-1. ANP reduced TNF-alpha-induced NF-kappaB activity, which was paralleled by a decreased translocation of p65 to nuclei. ANP did not alter TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, but attenuated degradation of IkappaB-epsilon. Moreover, ANP leads to a transcriptional induction of IkappaB-alpha. The induction of IkappaB by ANP is suggested as a novel mechanism for regulating inflammatory signalling in endothelial cells, leading to reduced TNF-alpha-induced expression of adhesion molecules
U2 - https://doi.org/10.1016/S0006-291X(02)00807-0
DO - https://doi.org/10.1016/S0006-291X(02)00807-0
M3 - Article
C2 - 12135603
SN - 0006-291X
VL - 295
SP - 1068
EP - 1076
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 5
ER -