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Critical role of nucleotide-binding oligomerization domain-like receptor 3 in vascular repair.

Abstract：

:Vascular remodeling characterized by hyperproliferative neointima formation is an unfavorable repair process that is triggered by vascular damage. This process is characterized by an increased local inflammatory and proliferative response that critically involves the pro-inflammatory cytokine interleukin-1β (IL-1β). IL-1β is expressed and cytosolically retained as a procytokine that requires additional processing prior to exerting its pro-inflammatory function. Maturation and release of pro IL-1β is governed by a cytosolic protein scaffold that is known as the inflammasome. Here we show that NLRP3 (NOD-like receptor family, pryin domain containing 3), an important activating component of the inflammasome, is involved in neointima formation after vascular injury. NLRP3 deficiency itself does not affect the functional cardiovascular phenotype and does not alter peripheral differential blood counts. However, neointima development following wire injury of the carotid artery was significantly decreased in NLRP3-deficient mice as compared to wild-type controls. In all, NLRP3 plays a non-redundant role in vascular damage mediated neointima formation. Our data establish NLRP3 as a key player in the response to vascular damage, which could open new avenues to therapeutic intervention.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Schlaweck S,Zimmer S,Struck R,Bartok E,Werner N,Bauernfeind F,Latz E,Nickenig G,Hornung V,Ghanem A

doi

10.1016/j.bbrc.2011.07.006

subject

Has Abstract

pub_date

2011-08-05 00:00:00

pages

627-31

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)01225-3

journal_volume

411

pub_type

杂志文章

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