Linked Life Data

21354814

Source:http://linkedlifedata.com/resource/pubmed/id/21354814

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-3-30
pubmed:abstractText
Adenosine receptor A3 (A3R) belongs to the Gi/Gq-coupled receptor family, that leads to the intracellular cAMP reduction and intracellular calcium increase, respectively. A3R is widely expressed and it can play a crucial role in many patho-physiological conditions, including inflammation. Here we investigate the effect of Cl-IB-MECA, A3R agonist, on the production of TNF-?. We found that Cl-IB-MECA enhances LPS-induced TNF-? release in peritoneal macrophages. This effect is reduced by MRS1191, A3R antagonist and by forskolin, activator of adenylyl cyclase. pI?B? increased in LPS+Cl-IB-MECA-treated macrophages, while total I?B kinase-? (IKK?) reduced. Indeed, p65NF-?B nuclear translocation increased in cells treated with LPS+Cl-IB-MECA. Moreover, IMD 0354, IKK? inhibitor, significantly abrogated the effect of Cl-IB-MECA on TNF-? release. Inhibition of protein kinase C (PKC) significantly reduced Cl-IB-MECA-induced TNF-? release in LPS-stimulated macrophages. Furthermore, LY-294002, PI3K inhibitor, reduced the TNF-? production enhanced by Cl-IB-MECA, although the phosphorylation status of Akt did not change in cells treated with LPS+Cl-IB-MECA than LPS alone. In summary, these data show that Cl-IB-MECA is able to enhance TNF-? production in LPS-treated macrophages in an NF-?B- dependent manner.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1096-0023
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
161-6
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Cl-IB-MECA enhances TNF-? release in peritoneal macrophages stimulated with LPS.
pubmed:affiliation
Department of Pharmaceutical Sciences, University of Salerno, Fisciano Salerno, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't