| http://purl.uniprot.org/citations/12960255 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12960255 | http://www.w3.org/2000/01/rdf-schema#comment | "Atrial natriuretic peptide (ANP) has been shown to reduce tumor necrosis factor-alpha (TNF-alpha)-induced activation of endothelial cells via inhibition of p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB pathways. The aim of this study was to determine whether ANP is able to inhibit TNF-alpha-induced expression of monocyte chemoattractant protein-1 (MCP-1) in endothelial cells and to elucidate the mechanisms involved. Pretreatment of human umbilical vein endothelial cells (HUVEC) with ANP significantly reduced TNF-alpha-induced expression of MCP-1 protein and mRNA. The effects of ANP were shown to be mediated via the guanylyl-cyclase (GC)-coupled A receptor. Activation of the other GC-coupled receptor (natriuretic peptide receptor-B) by the C-type natriuretic peptide as well as activation of soluble GC with S-nitroso-L-glutathione (GSNO) exerted similar effects as ANP, supporting a role for cyclic guanosine monophosphate (cGMP) in the signal transduction. Antisense experiments showed a requirement of MAPK phosphatase-1 (MKP-1) induction and therefore, inhibition of p38 MAPK in the ANP-mediated inhibition of TNF-alpha-induced expression of MCP-1. To investigate a potential interplay between TNF-alpha-induced activation of p38 MAPK and NF-kappaB, the p38 MAPK inhibitor SB203580 and a dominant-negative p38 MAPK mutant were used. The results indicated that the blockade of p38 MAPK activity leads to an increased activation of NF-kappaB and therefore, suggest a counter-regulatory action of p38 MAPK and NF-kappaB. As antisense experiments revealed a pivotal role for MKP-1 induction and therefore, p38 MAPK inhibition in ANP-mediated attenuation of MCP-1 expression, this action seems to be rather independent of NF-kappaB inhibition."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.org/dc/terms/identifier | "doi:10.1189/jlb.0603254"xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/author | "Hartung T."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/author | "Vollmar A.M."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/author | "Kiemer A.K."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/author | "Weber N.C."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/author | "Blumenthal S.B."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/name | "J Leukoc Biol"xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/pages | "932-941"xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/title | "ANP inhibits TNF-alpha-induced endothelial MCP-1 expression--involvement of p38 MAPK and MKP-1."xsd:string |
| http://purl.uniprot.org/citations/12960255 | http://purl.uniprot.org/core/volume | "74"xsd:string |
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