Release of mitochondrial DNA fragments from brain mitochondria of irradiated mice

Патрушев, М. В.; Kasymov, Vitaliy; Патрушева, В. Е.; Ushakova, T. N.; Gogvadze, Vladimir; Gaziev, A.I.

doi:10.1016/j.mito.2005.12.001

Cited by 46 publications

(30 citation statements)

References 25 publications

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“…This mechanism for DNA release has also been demonstrated by Patrushev et al (2004). Recently, they demonstrated that mitochondrial DNA release can happen in vivo; they discussed the above based on the fact that mitochondrial DNA fragments are found in the cytosol fraction when mice are exposed to radiation (Patrushev et al, 2006).…”

Section: Resultsmentioning

confidence: 68%

Mitochondrial DNA fragments released through the permeability transition pore correspond to specific gene size

Garcı́a

Chávez

2007

Life Sciences

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Section: Resultsmentioning

confidence: 68%

Mitochondrial DNA fragments released through the permeability transition pore correspond to specific gene size

Garcı́a

Chávez

2007

Life Sciences

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“…Patrushev et al . reported that mtDNA is released into the cytosol during intrinsic apoptosis (Patrushev et al, 2006). Thus, we hypothesized that mtDNA released into the cytosol during apoptosis might trigger NLRP3 inflammasome activation.…”

Section: Resultsmentioning

confidence: 99%

Oxidized Mitochondrial DNA Activates the NLRP3 Inflammasome during Apoptosis

et al. 2012

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SUMMARY We report that in the presence of signal 1 (NF-κB), the NLRP3 inflammasome was activated by mitochondrial apoptotic signaling that licensed production of interleukin-1β (IL-1β). NLRP3 secondary signal activators such as ATP induced mitochondrial dysfunction and apoptosis, resulting in release of oxidized mitochondrial DNA (mtDNA) into the cytosol, where it bound to and activated the NLRP3 inflammasome. The anti-apoptotic protein Bcl-2 inversely regulated mitochondrial dysfunction and NLRP3 inflammasome activation. Mitochondrial DNA directly induced NLRP3 inflammasome activation, because macrophages lacking mtDNA had severely attenuated IL-1β production, yet still underwent apoptosis. Both binding of oxidized mtDNA to the NLRP3 inflammasome and IL-1β secretion could be competitively inhibited by the oxidized nucleoside, 8-OH-dG. Thus, our data reveal that oxidized mtDNA released during programmed cell death causes activation of the NLRP3 inflammasome. These results provide a missing link between apoptosis and inflammasome activation, via binding of cytosolic oxidized mtDNA to the NLRP3 inflammasome.

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“…Similarly, self and foreign DNA in the cytoplasm have also been shown to activate the AIM2 inflammasome [54, 55]. Mitochondrial DNA is released into the cytoplasm following intrinsic cell death, resulting in inflammation [56, 57]. Following on from these reports, two separate studies have now shown that mitochondrial DNA in the cytoplasm activates the NLRP3 inflammasome [17, 58].…”

Section: Mitochondria Inflammation and Regulation Of The Nlrp3 Inflamentioning

confidence: 99%

Mitochondria: diversity in the regulation of the NLRP3 inflammasome

Gurung

Lukens

Kanneganti

2015

Trends in Molecular Medicine

333

227

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Recent studies have identified new roles for mitochondria in the regulation of autoinflammatory processes. Emerging data suggests that the release of danger signals from mitochondria in response to stress and infection promotes the formation of the inflammatory signaling platform known as inflammasomes. Activation of inflammasomes by damaged mitochondria results in caspase-1-dependent secretion of the inflammatory cytokines IL-1β and IL-18, and an inflammatory form of cell death referred to as pyroptosis. Here, we review recently described mechanisms that have been proposed to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation. In addition, we highlight how aberrant regulation of mitochondria-induced inflammasome activation centrally contributes to the inflammatory process that are responsible for obesity and associated metabolic diseases.

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Release of mitochondrial DNA fragments from brain mitochondria of irradiated mice

Cited by 46 publications

References 25 publications

Mitochondrial DNA fragments released through the permeability transition pore correspond to specific gene size

Mitochondrial DNA fragments released through the permeability transition pore correspond to specific gene size

Oxidized Mitochondrial DNA Activates the NLRP3 Inflammasome during Apoptosis

Mitochondria: diversity in the regulation of the NLRP3 inflammasome

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