Mitochondria-associated membranes (MAMs) and inflammation

Missiroli, Sonia; Patergnani, Simone; Caroccia, Natascia; Pedriali, Gaia; Perrone, Mariasole; Previati, Maurizio; Wieckowski, Mariusz R.; Giorgi, Carlotta

doi:10.1038/s41419-017-0027-2

Cited by 223 publications

(205 citation statements)

References 129 publications

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“…A link between the ERMES complex and inflammation was recognized earlier and later observed by Zhou et al . Currently, NLRP3 complex is the only inflammatory complex that is associated with MAM .…”

Section: Er–mitochondria Crosstalk Functionalitiesmentioning

confidence: 68%

“…studied that inflammatory microtubules drive perinuclear migration of mitochondria resulting in ensuing apposition of ASC on mitochondria to NLRP3 on the ER . Thus, upon activation of its ER–mitochondria localization, the NLRP3 inflammasome is strategically positioned to perceive the signals emanating from the mitochondria …”

Section: Er–mitochondria Crosstalk Functionalitiesmentioning

confidence: 99%

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Endoplasmic reticulum–mitochondria crosstalk: from junction to function across neurological disorders

Veeresh

Kaur

Sarmah

et al. 2019

Annals of the New York Academy of Sciences

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The endoplasmic reticulum (ER) and mitochondria are fundamental organelles highly interconnected with a specialized set of proteins in cells. ER–mitochondrial interconnections form specific microdomains, called mitochondria‐associated ER membranes, that have been found to play important roles in calcium signaling and lipid homeostasis, and more recently in mitochondrial dynamics, inflammation, and autophagy. It is not surprising that perturbations in ER–mitochondria connections can result in the progression of disease, especially neurological disorders; hence, their architecture and regulation are crucial in determining the fate of cells and disease. The molecular identity of the specialized proteins regulating ER–mitochondrial crosstalk remains unclear. Our discussion here describes the physical and functional crosstalk between these two dynamic organelles and emphasizes the outcome of altered ER–mitochondrial interconnections in neurological disorders.

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Section: Er–mitochondria Crosstalk Functionalitiesmentioning

confidence: 68%

Section: Er–mitochondria Crosstalk Functionalitiesmentioning

confidence: 99%

Endoplasmic reticulum–mitochondria crosstalk: from junction to function across neurological disorders

Veeresh

Kaur

Sarmah

et al. 2019

Annals of the New York Academy of Sciences

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“…A relevant point to be approached in the continuity of this research is a strongly associated relationship between endoplasmic reticulum and mitochondria since an association between membranes that facilitate the communication between these organelles, demonstrating an essential role in different inflammatory signaling pathways allowed a rapid exchange of biological molecules to maintain health and cellular integrity. The dysfunctions in architecture of reticulum and mitochondria may be associated with pathological conditions (Missiroli et al, 2018; Jou et al, 2007). We verified in our study that electron microscopy results of Met group visually changes in both organelles.…”

Section: Discussionmentioning

confidence: 99%

The neuroprotective role of melatonin in a gestational hypermethioninemia model

Figueiró¹,

Moreira²,

Santos³

et al. 2019

Intl J of Devlp Neuroscience

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Elevated levels of methionine in blood characterize the hypermethioninemia, which may have genetic or non‐genetic origin, as for example from high protein diet. Born rats from hypermethioninemic mothers presented cerebral oxidative stress, inhibition of Na+,K+‐ATPase, memory deficit and ultrastructure cerebral changes. Melatonin is a hormone involved in circadian rhythm and has antioxidant effects. The aim of this study was to verify the possible neuroprotective effects of melatonin administration in hypermethioninemic pregnant rats on damage to biomolecules (Na+,K+‐ATPase, sulfhydryl content and DNA damage index) and behavior (open field, novel object recognition and water maze tasks), as well as its effect on cells morphology by electron microscopy in offspring. Wistar female rats received methionine (2.68 μmol/g body weight) and/or melatonin (10 mg/kg body weight) by subcutaneous injections during entire pregnancy. Control rats received saline. Biochemical analyzes were performed at 21 and 30 days of life of offspring and behavioral analyzes were performed only at 30 days of age in male pups. Results showed that gestational hypermethioninemia diminished Na+,K+‐ATPase activity and sulfhydryl content and increased DNA damage at 21 and 30 days of life. Melatonin was able to totally prevent Na+,K+‐ATPase activity alteration at 21 days and partially prevent its alteration at 30 days of rats life. Melatonin was unable in to prevent sulfhydryl and DNA damage at two ages. It also improved DNA damage, but not at level of saline animals (controls). Regarding to behavioral tests, data showed that pups exposed to gestational hypermethioninemia decreased reference memory in water maze, spent more time to the center of the open field and did not differentiate the objects in the recognition test. Melatonin was able to prevent the deficit in novel object recognition task. Electron microscopy revealed ultrastructure alterations in neurons of hypermethioninemic at both ages of offspring, whose were prevented by melatonin. These findings suggest that melatonin may be a good neuroprotective to minimize the harmful effects of gestational hypermethioninemia on offspring.

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“…MAMs are emerging as important signalling hubs between the ER and mitochondria and are a possible site of NLRP3 inflammasome assembly. 55 It is possible that LLO-driven MAM disruption and mitochondrial fission removes a key site of inflammasome assembly to dampen K + effluxdependent NLRP3 signalling and thereby allows the bacterium to partially evade immune recognition.…”

Section: Bacterial Infectionmentioning

confidence: 99%

The rOX‐stars of inflammation: links between the inflammasome and mitochondrial meltdown

Holley

Schroder

2020

Clin & Trans Imm

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The nod-like receptor protein 3 (NLRP3) inflammasome drives inflammation in response to mitochondrial dysfunction. As metabolic powerhouses with prokaryotic ancestry, mitochondria are a cache for danger-associated molecular patterns and pathogen-associated molecular pattern-like molecules that elicit potent innate immune responses. Persistent mitochondrial damage caused by infection, or genetic or environmental factors, can lead to inappropriate or sustained inflammasome signalling. Here, we review the features of mitochondria that drive inflammatory signalling, with a particular focus on mitochondrial activation of the NLRP3 inflammasome. Given that mitochondrial network dynamics, metabolic activity and redox state are all intricately linked to each other and to NLRP3 inflammasome activity, we highlight the importance of a holistic approach to investigations of NLRP3 activation by dysfunctional mitochondria.

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Mitochondria-associated membranes (MAMs) and inflammation

Cited by 223 publications

References 129 publications

Endoplasmic reticulum–mitochondria crosstalk: from junction to function across neurological disorders

Endoplasmic reticulum–mitochondria crosstalk: from junction to function across neurological disorders

The neuroprotective role of melatonin in a gestational hypermethioninemia model

The rOX‐stars of inflammation: links between the inflammasome and mitochondrial meltdown

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