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

Schlaweck, Sebastian; Zimmer, Sebastian; Struck, Rafael; Bartok, Eva; Werner, Nikos; Bauernfeind, Franz; Latz, Eicke; Nickenig, Georg; Hornung, Veit; Ghanem, Alexander

doi:10.1016/J.BBRC.2011.07.006

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

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Abstract

Highlights: {yields} NLRP3 is not required for systemic cardiovascular function in healthy mice. {yields} NLRP3 deficiency itself does not affect the functional cardiovascular phenotype and that it does not alter peripheral differential blood counts. {yields} NLRP3 is critical in neointima formation following vascular injury. -- 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-1{beta} (IL-1{beta}). IL-1{beta} 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-1{beta} 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 neointimamore »« less

Authors:

Schlaweck, Sebastian; Zimmer, Sebastian; Struck, Rafael ^[1]; Bartok, Eva ^[2]; Werner, Nikos ^[1]; Bauernfeind, Franz ^[2]; Latz, Eicke ^[3]; Nickenig, Georg ^[1]; Hornung, Veit ^[2]; Ghanem, Alexander ^[1]

Department of Medicine/Cardiology, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn (Germany)
Institute for Clinical Chemistry and Clinical Pharmacology, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn (Germany)
Institute of Innate Immunity, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn (Germany)

Publication Date:: Fri Aug 05 00:00:00 EDT 2011

OSTI Identifier:: 22207429

Resource Type:: Journal Article

Journal Name:: Biochemical and Biophysical Research Communications

Additional Journal Information:: Journal Volume: 411; Journal Issue: 3; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; BLOOD COUNT; CAROTID ARTERIES; DNA DAMAGES; DNA REPAIR; INFLAMMATION; INJURIES; MICE; NUCLEOTIDES; PHENOTYPE; RECEPTORS

Citation Formats


                    Schlaweck, Sebastian, Zimmer, Sebastian, Struck, Rafael, Bartok, Eva, Werner, Nikos, Bauernfeind, Franz, Latz, Eicke, Nickenig, Georg, Hornung, Veit, and Ghanem, Alexander. Critical role of nucleotide-binding oligomerization domain-like receptor 3 in vascular repair.  United States: N. p., 2011. 
        Web.  doi:10.1016/J.BBRC.2011.07.006.

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                    Schlaweck, Sebastian, Zimmer, Sebastian, Struck, Rafael, Bartok, Eva, Werner, Nikos, Bauernfeind, Franz, Latz, Eicke, Nickenig, Georg, Hornung, Veit, & Ghanem, Alexander. Critical role of nucleotide-binding oligomerization domain-like receptor 3 in vascular repair.  United States.  https://doi.org/10.1016/J.BBRC.2011.07.006

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                    Schlaweck, Sebastian, Zimmer, Sebastian, Struck, Rafael, Bartok, Eva, Werner, Nikos, Bauernfeind, Franz, Latz, Eicke, Nickenig, Georg, Hornung, Veit, and Ghanem, Alexander. 2011.  
        "Critical role of nucleotide-binding oligomerization domain-like receptor 3 in vascular repair".  United States.  https://doi.org/10.1016/J.BBRC.2011.07.006.

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@article{osti_22207429,

  title        = {Critical role of nucleotide-binding oligomerization domain-like receptor 3 in vascular repair},

  author       = {Schlaweck, Sebastian and Zimmer, Sebastian and Struck, Rafael and Bartok, Eva and Werner, Nikos and Bauernfeind, Franz and Latz, Eicke and Nickenig, Georg and Hornung, Veit and Ghanem, Alexander},

  abstractNote = {Highlights: {yields} NLRP3 is not required for systemic cardiovascular function in healthy mice. {yields} NLRP3 deficiency itself does not affect the functional cardiovascular phenotype and that it does not alter peripheral differential blood counts. {yields} NLRP3 is critical in neointima formation following vascular injury. -- 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-1{beta} (IL-1{beta}). IL-1{beta} 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-1{beta} 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.},

  doi          = {10.1016/J.BBRC.2011.07.006},

  url          = {https://www.osti.gov/biblio/22207429},
  journal      = {Biochemical and Biophysical Research Communications},

  issn         = {0006-291X},

  number       = 3,

  volume       = 411,

  place        = {United States},

  year         = {Fri Aug 05 00:00:00 EDT 2011},

  month        = {Fri Aug 05 00:00:00 EDT 2011}

}

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