%0 Journal Article %1 Henke.2007 %A Henke, N. %A Schmidt-Ullrich, R. %A Dechend, R. %A Park, J. K. %A Qadri, F. %A Wellner, M. %A Obst, M. %A Gross, V. %A Dietz, R. %A Luft, F. C. %A Scheidereit, C. %A Muller, D. N. %D 2007 %J Circ.Res. %K & Adhesion Albuminuria Angiotensin Animals Atherosclerosis B Blood C57BL Cardiovascular Cell Cells Chain Chloride Cultured Dietary Diseases Endothelial Ester Expression Factor-alpha Fusion Gene Humans Hypertension I-kappa II III Inbred Inflammation Intercellular Kidney Methyl Mice Models Molecule-1 NF-kappa NG-Nitroarginine Necrosis Nephritis Nitric Organ Oxide Polymerase Pressure Proteins Reaction Receptor Recombinant Regulation Research Reverse Signal Sodium Specificity Synthase TIE-1 Transcriptase Transduction Transgenic Tumor Type Vascular antagonists biosynthesis blood cells complications control etiology genetics inhibitors metabolism physiology physiopathology prevention protein toxicity %N 3 %P 268-276 %T Vascular endothelial cell-specific NF-kappaB suppression attenuates hypertension-induced renal damage %U PM:17585070 %V 101 %X Nuclear factor kappa B (NF-kappaB) participates in hypertension-induced vascular and target-organ damage. We tested whether or not endothelial cell-specific NF-kappaB suppression would be ameliorative. We generated Cre/lox transgenic mice with endothelial cell-restricted NF-kappaB super-repressor IkappaBalphaDeltaN (Tie-1-DeltaN mice) overexpression. We confirmed cell-specific IkappaBalphaDeltaN expression and reduced NF-kappaB activity after TNF-alpha stimulation in primary endothelial cell culture. To induce hypertension with target-organ damage, we fed mice a high-salt diet and N(omega)-nitro-l-arginine-methyl-ester (L-NAME) and infused angiotensin (Ang) II. This treatment caused a 40-mm Hg blood pressure increase in both Tie-1-DeltaN and control mice. In contrast to control mice, Tie-1-DeltaN mice developed a milder renal injury, reduced inflammation, and less albuminuria. RT-PCR showed significantly reduced expression of the NF-kappaB targets VCAM-1 and ICAM-1, compared with contr

@article{Henke.2007, abstract = {Nuclear factor kappa B (NF-kappaB) participates in hypertension-induced vascular and target-organ damage. We tested whether or not endothelial cell-specific NF-kappaB suppression would be ameliorative. We generated Cre/lox transgenic mice with endothelial cell-restricted NF-kappaB super-repressor IkappaBalphaDeltaN (Tie-1-DeltaN mice) overexpression. We confirmed cell-specific IkappaBalphaDeltaN expression and reduced NF-kappaB activity after TNF-alpha stimulation in primary endothelial cell culture. To induce hypertension with target-organ damage, we fed mice a high-salt diet and N(omega)-nitro-l-arginine-methyl-ester (L-NAME) and infused angiotensin (Ang) II. This treatment caused a 40-mm Hg blood pressure increase in both Tie-1-DeltaN and control mice. In contrast to control mice, Tie-1-DeltaN mice developed a milder renal injury, reduced inflammation, and less albuminuria. RT-PCR showed significantly reduced expression of the NF-kappaB targets VCAM-1 and ICAM-1, compared with contr}, added-at = {2010-02-05T11:28:39.000+0100}, author = {Henke, N. and Schmidt-Ullrich, R. and Dechend, R. and Park, J. K. and Qadri, F. and Wellner, M. and Obst, M. and Gross, V. and Dietz, R. and Luft, F. C. and Scheidereit, C. and Muller, D. N.}, biburl = {https://www.bibsonomy.org/bibtex/2fe9b6da17080b89b77fd623f65128cf0/kanefendt}, interhash = {1d7a9e91c5ca7cb2f5638229c605fa21}, intrahash = {fe9b6da17080b89b77fd623f65128cf0}, journal = {Circ.Res.}, keywords = {& Adhesion Albuminuria Angiotensin Animals Atherosclerosis B Blood C57BL Cardiovascular Cell Cells Chain Chloride Cultured Dietary Diseases Endothelial Ester Expression Factor-alpha Fusion Gene Humans Hypertension I-kappa II III Inbred Inflammation Intercellular Kidney Methyl Mice Models Molecule-1 NF-kappa NG-Nitroarginine Necrosis Nephritis Nitric Organ Oxide Polymerase Pressure Proteins Reaction Receptor Recombinant Regulation Research Reverse Signal Sodium Specificity Synthase TIE-1 Transcriptase Transduction Transgenic Tumor Type Vascular antagonists biosynthesis blood cells complications control etiology genetics inhibitors metabolism physiology physiopathology prevention protein toxicity}, number = 3, pages = {268-276}, timestamp = {2010-02-05T11:28:57.000+0100}, title = {Vascular endothelial cell-specific NF-kappaB suppression attenuates hypertension-induced renal damage}, url = {PM:17585070}, volume = 101, year = 2007 }