Circulation Research. 2002
Published online before print April 4, 2002, doi: 10.1161/01.RES.0000017068.58856.F3
Published online before print April 4, 2002, doi: 10.1161/01.RES.0000017068.58856.F3
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Submitted on October 31, 2001
Revised on March 20, 2002
Accepted on March 20, 2002
Inhibition of p38 MAPK Activation via Induction of MKP-1. Atrial Natriuretic Peptide Reduces TNF-
--Induced Actin Polymerization and Endothelial Permeability
Alexandra K. Kiemer *;
From the Department of Pharmacy, Center of Drug Research, University of Munich, Munich, Germany.
* To whom correspondence should be addressed. E-mail: Alexandra.Kiemer{at}cup.uni-muenchen.de.
The atrial natriuretic peptide (ANP) is a cardiovascular hormone possessing antiinflammatory potential due to its inhibitory action on the production of inflammatory mediators, such as tumor necrosis factor- (TNF-). The aim of this study was to determine whether ANP is able to attenuate inflammatory effects of TNF- on target cells. Human umbilical vein endothelial cells (HUVECs) were treated with TNF- in the presence or absence of ANP. Changes in permeability, cytoskeletal alterations, phosphorylation of p38 MAPK and HSP27, and expression of MKP-1 were determined by macromolecule permeability assay, fluorescence labeling, RT-PCR, and immunoblotting. Antisense studies were done by transfecting cells with MKP-1 antisense oligonucleotides. Activation of HUVECs with TNF- lead to a significant increase of macromolecule permeability and formation of stress fibers. Treatment of cells with ANP (10-8 to 10-6 mol/L) significantly reduced the formation of stress fibers and elevated permeability. Both TNF---induced effects were shown to be mediated via the activation of p38 using SB203580, a specific inhibitor of p38. ANP significantly reduced the TNF---induced activation of p38 and attenuated the phosphorylation of HSP27, a central target downstream of p38. ANP showed no effect on p38 upstream kinases MKK3/6. However, a significant induction of the MAPK phosphatase MKP-1 mRNA and protein could be observed in ANP-treated cells. Antisense experiments proved a causal role for MKP-1 induction in the ANP-mediated inhibition of p38. These data show the inhibitory action of ANP on TNF---induced changes in endothelial cytoskeleton and macromolecule permeability involving an MKP-1--induced inactivation of p38 MAPK. These effects point to an antiinflammatory and antiatherogenic potential of this cardiovascular hormone.
Key words: signal transduction • inflammation • endothelium • hormones • natriuretic peptides
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