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The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury
Cardiovascular research, 2013-07, Vol.99 (1), p.164-174
[Peer Reviewed Journal]
ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvt091 ;PMID: 23580606
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Title:
The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia-reperfusion injury
Author:
Sandanger, Øystein
;
Ranheim, Trine
;
Vinge, Leif Erik
;
Bliksøen, Marte
;
Alfsnes, Katrine
;
Finsen, Alexandra V
;
Dahl, Christen P
;
Askevold, Erik T
;
Florholmen, Geir
;
Christensen, Geir
;
Fitzgerald, Katherine A
;
Lien, Egil
;
Valen, Guro
;
Espevik, Terje
;
Aukrust, Pål
;
Yndestad, Arne
Subjects:
Adenosine Triphosphate - metabolism
;
Animals
;
Apoptosis
;
Apoptosis Regulatory Proteins
;
CARD Signaling Adaptor Proteins
;
Carrier Proteins - genetics
;
Carrier Proteins - metabolism
;
Caspase 1 - metabolism
;
Cells, Cultured
;
Cytoskeletal Proteins - deficiency
;
Cytoskeletal Proteins - genetics
;
Disease Models, Animal
;
Fibroblasts - drug effects
;
Fibroblasts - immunology
;
Fibroblasts - metabolism
;
Heart Ventricles - drug effects
;
Heart Ventricles - immunology
;
Heart Ventricles - metabolism
;
Heart Ventricles - pathology
;
Heart Ventricles - physiopathology
;
Inflammasomes - genetics
;
Inflammasomes - metabolism
;
Interleukin-18 - genetics
;
Interleukin-18 - metabolism
;
Interleukin-1beta - genetics
;
Interleukin-1beta - metabolism
;
Lipopolysaccharides - pharmacology
;
Male
;
Mice
;
Mice, Inbred C57BL
;
Mice, Knockout
;
Myocardial Contraction
;
Myocardial Infarction - genetics
;
Myocardial Infarction - immunology
;
Myocardial Infarction - metabolism
;
Myocardial Infarction - pathology
;
Myocardial Infarction - physiopathology
;
Myocardial Reperfusion Injury - genetics
;
Myocardial Reperfusion Injury - immunology
;
Myocardial Reperfusion Injury - metabolism
;
Myocardial Reperfusion Injury - pathology
;
Myocardial Reperfusion Injury - physiopathology
;
Myocardial Reperfusion Injury - prevention & control
;
NF-kappa B - metabolism
;
NLR Family, Pyrin Domain-Containing 3 Protein
;
Potassium - metabolism
;
Rats
;
Rats, Wistar
;
Receptors, Cytoplasmic and Nuclear - genetics
;
Receptors, Cytoplasmic and Nuclear - metabolism
;
RNA, Messenger - metabolism
;
Time Factors
;
Toll-Like Receptors - metabolism
;
Up-Regulation
;
Ventricular Function, Left
Is Part Of:
Cardiovascular research, 2013-07, Vol.99 (1), p.164-174
Description:
Nucleotide-binding oligomerization domain-Like Receptor with a Pyrin domain 3 (NLRP3) is considered necessary for initiating a profound sterile inflammatory response. NLRP3 forms multi-protein complexes with Apoptosis-associated Speck-like protein containing a Caspase recruitment domain (ASC) and Caspase-1, which activate pro-interleukin-1β (IL-1β) and pro-IL-18. The role of NLRP3 in cardiac cells is not known. Thus, we investigated the expression and function of NLRP3 during myocardial ischaemia. Myocardial infarction (MI) was induced in adult C57BL/6 mice and Wistar rats by ligation of the coronary artery. A marked increase in NLRP3, IL-1β, and IL-18 mRNA expression was found in the left ventricle after MI, primarily located to myocardial fibroblasts. In vitro studies in cells from adult mice showed that myocardial fibroblasts released IL-1β and IL-18 when primed with lipopolysaccharide and subsequently exposed to the danger signal adenosine triphosphate, a molecule released after tissue damage during MI. When hearts were isolated from NLRP3-deficient mice, perfused and subjected to global ischaemia and reperfusion, a marked improvement of cardiac function and reduction of hypoxic damage was found compared with wild-type hearts. This was not observed in ASC-deficient hearts, potentially reflecting a protective role of other ASC-dependent inflammasomes or inflammasome-independent effects of NLRP3. This study shows that the NLRP3 inflammasome is up-regulated in myocardial fibroblasts post-MI, and may be a significant contributor to infarct size development during ischaemia-reperfusion.
Publisher:
England
Language:
English
Identifier:
ISSN: 0008-6363
EISSN: 1755-3245
DOI: 10.1093/cvr/cvt091
PMID: 23580606
Source:
Geneva Foundation Free Medical Journals at publisher websites
MEDLINE
Alma/SFX Local Collection
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