Measurement of Cytosolic Mitochondrial DNA After NLRP3 Inflammasome Activation.


Journal

Methods in molecular biology (Clifton, N.J.)
ISSN: 1940-6029
Titre abrégé: Methods Mol Biol
Pays: United States
ID NLM: 9214969

Informations de publication

Date de publication:
2022
Historique:
entrez: 25 2 2022
pubmed: 26 2 2022
medline: 3 3 2022
Statut: ppublish

Résumé

The NLRP3 inflammasome, a key component of the innate immune system that mediates caspase-1 activation, which in turn induces cleavage of the pyroptosis executioner gasdermin D and the proinflammatory cytokines IL-1β and IL-18, requires two signals to be activated. First, inflammasome priming is achieved after activation of Toll-like receptors, which leads to NF-κB signaling and transcriptional activation of the genes for NLRP3 and IL-1β. Next, the inflammasome complex is activated by a second signal that induces extrusion of mitochondrial DNA to the cytosol of the cell, which leads to its oligomerization by a not fully understood mechanism. Here we describe a simple method that employs quantitative polymerase chain reaction (qPCR) using SYBR green to measure the presence of mitochondrial DNA (mtDNA) in the cytosol, which can be used to measure cytosolic mtDNA levels after inflammasome activation.

Identifiants

pubmed: 35212960
doi: 10.1007/978-1-0716-2144-8_12
doi:

Substances chimiques

DNA, Mitochondrial 0
Inflammasomes 0
Interleukin-1beta 0
NLR Family, Pyrin Domain-Containing 3 Protein 0
Caspase 1 EC 3.4.22.36

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

117-129

Informations de copyright

© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.

Références

Strowig T, Henao-Mejia J, Elinav E et al (2012) Inflammasomes in health and disease. Nature 481(7381):278–286
doi: 10.1038/nature10759
Zhou R, Yazdi AS, Menu P et al (2011) A role for mitochondria in NLRP3 inflammasome activation. Nature 469(7329):221–225
doi: 10.1038/nature09663
Iyer SS, He Q, Janczy JR et al (2013) Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation. Immunity 39(2):311–323
doi: 10.1016/j.immuni.2013.08.001
Heid ME, Keyel PA, Kamga C et al (2013) Mitochondrial reactive oxygen species induces NLRP3-dependent lysosomal damage and inflammasome activation. J Immunol 191(10):5230–5238
doi: 10.4049/jimmunol.1301490
Nakahira K, Haspel JA, Rathinam VA et al (2011) Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome. Nat Immunol 12(3):222–230
doi: 10.1038/ni.1980
Shimada K, Crother TR, Karlin J et al (2012) Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. Immunity 36(3):401–414
doi: 10.1016/j.immuni.2012.01.009
Zhong Z, Liang S, Sanchez-Lopez E et al (2018) New mitochondrial DNA synthesis enables NLRP3 inflammasome activation. Nature 560(7717):198–203
doi: 10.1038/s41586-018-0372-z
Kim J, Gupta R, Blanco LP et al (2019) VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease. Science 366(6472):1531–1536
doi: 10.1126/science.aav4011
Patrushev M, Kasymov V, Patrusheva V et al (2004) Mitochondrial permeability transition triggers the release of mtDNA fragments. Cell Mol Life Sci 61(24):3100–3103
doi: 10.1007/s00018-004-4424-1
West AP, Khoury-Hanold W, Staron M et al (2015) Mitochondrial DNA stress primes the antiviral innate immune response. Nature 520(7548):553–557
doi: 10.1038/nature14156
Rodriguez-Nuevo A, Diaz-Ramos A, Noguera E et al (2018) Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency. EMBO J 37(10):e96553
doi: 10.15252/embj.201796553
Bae JH, Jo SI, Kim SJ et al (2019) Circulating cell-free mtDNA contributes to AIM2 Inflammasome-mediated chronic inflammation in patients with type 2 diabetes. Cell 8(4):328
doi: 10.3390/cells8040328
Traba J, Geiger SS, Kwarteng-Siaw M et al (2017) Prolonged fasting suppresses mitochondrial NLRP3 inflammasome assembly and activation via SIRT3-mediated activation of superoxide dismutase 2. J Biol Chem 292(29):12153–12164
doi: 10.1074/jbc.M117.791715
Li Y, Shen Y, Jin K et al (2019) The DNA repair nuclease MRE11A functions as a mitochondrial protector and prevents T cell Pyroptosis and tissue inflammation. Cell Metab 30(3):477–492.e6
doi: 10.1016/j.cmet.2019.06.016

Auteurs

Olga M Antón (OM)

Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute (NIH), Bethesda, MD, USA.

Javier Traba (J)

Departamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain. jtraba@cbm.csic.es.

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Classifications MeSH