Increased plasma levels of mitochondrial DNA and pro-inflammatory cytokines in patients with progressive multiple sclerosis

Nasi, Milena; Bianchini, Elena; Biasi, Sara De; Gibellini, Lara; Neroni, Anita; Mattioli, Marco; Iannone, Anna; Mattioli, Anna Vittoria; Simone, Anna Maria; Ferraro, Diana; Vitetta, Francesca; Sola, Patrizia; Cossarizza, Andrea

doi:10.1016/j.jneuroim.2019.577107

Cited by 19 publications

(13 citation statements)

References 27 publications

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“…Velders et al highlighted that even a single bout of high-intensity exercise, in healthy people, can enhance circulating DNase activity [73]. Otherwise, cf-mtDNA may be removed via the liver, spleen, or kidney [62,75]. In septic patients with kidney injuries, cf-mtDNA levels are elevated in urine but not in plasma, supporting the idea that urine is a possible mechanism of cf-mtDNA elimination [76].…”

Section: Release Forms and Detection Of Cf-mtdna 41 Mechanisms Of Release And Removal Of Cf-mtdnamentioning

confidence: 99%

Mitochondrial DNA and Exercise: Implications for Health and Injuries in Sports

Zanini

Gaetano

Selleri

et al. 2021

Cells

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Recently, several studies have highlighted the tight connection between mitochondria and physical activity. Mitochondrial functions are important in high-demanding metabolic activities, such as endurance sports. Moreover, regular training positively affects metabolic health by increasing mitochondrial oxidative capacity and regulating glucose metabolism. Exercise could have multiple effects, also on the mitochondrial DNA (mtDNA) and vice versa; some studies have investigated how mtDNA polymorphisms can affect the performance of general athletes and mtDNA haplogroups seem to be related to the performance of elite endurance athletes. Along with several stimuli, including pathogens, stress, trauma, and reactive oxygen species, acute and intense exercise also seem to be responsible for mtDNA release into the cytoplasm and extracellular space, leading to the activation of the innate immune response. In addition, several sports are characterized by a higher frequency of injuries, including cranial trauma, associated with neurological consequences. However, with regular exercise, circulating cell-free mtDNA levels are kept low, perhaps promoting cf-mtDNA removal, acting as a protective factor against inflammation.

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Section: Release Forms and Detection Of Cf-mtdna 41 Mechanisms Of Release And Removal Of Cf-mtdnamentioning

confidence: 99%

Mitochondrial DNA and Exercise: Implications for Health and Injuries in Sports

Zanini

Gaetano

Selleri

et al. 2021

Cells

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“…Peripheral blood mononuclear cells (PBMC) and plasma were isolated from up to 20 ml of venous blood by density gradient centrifugation, using standardized protocols and Lymphoprep reagent from Stemcell (Cambridge, MA, United States). Plasma was then stored at −80 • C until use (10). A minimum of 1.5 million CD14+ monocytes were sorted starting from 20 million PBMC through immunomagnetic separation technique (Miltenyi Biotec, Bergish Gladbach, Germany).…”

Section: Biological Sample Collection Processing and Storagementioning

confidence: 99%

Increased Plasma Levels of Mitochondrial DNA and Normal Inflammasome Gene Expression in Monocytes Characterize Patients With Septic Shock Due to Multidrug Resistant Bacteria

et al. 2020

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“…One microliter of DNA was added to a 20 μL final volume mixture containing 10 μL of 2× ddPCR Supermix for Probes, 1 μL of ddPCR assay for ND4 (UniqueAssayID: dHsaCPE5043566), 1 μL of ddPCR assay for Actb (UniqueAssayID: dHsaCNS141996500) and 7 μL of nuclease-free water (all reagents from Bio-Rad, Hercules, CA, USA). Droplet generation and reading were performed on a Bio-Rad QX200 ddPCR droplet system [ 46 ]. Data are expressed as number of copies of mtDNA/nuclear equivalents.…”

Section: Methodsmentioning

confidence: 99%

Mitochondrial and Endoplasmic Reticulum Alterations in a Case of Amyotrophic Lateral Sclerosis Caused by TDP-43 A382T Mutation

Zanini

Selleri

Nasi

et al. 2022

IJMS

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Amyotrophic lateral sclerosis is the most common form of motor neuron disease. Mutations in TARDBP, the gene encoding the RNA-binding protein TDP-43, are responsible for about 5% of familial ALS. Here we report the clinical and biological features of an ALS patients with pA382T mutation in TPD-43 protein. Disease began with right hand muscles weakness, and equally involved upper and lower motor neuron with a classic phenotype, without cognitive impairment. While a family history of neurological diseases was reported, there was no evidence of familial frontotemporal dementia. Cultured fibroblasts from the patient were characterized by profound alterations of cell proteome, which impacts particularly the mitochondrial metabolic pathways and the endoplasmic reticulum. TDP-43 levels were similar to control, healthy fibroblasts, but a higher fraction localized in mitochondria. Mitochondrial network appeared fragmented, and the organelles smaller and more spheric. In agreement with impaired proteome and morphology of mitochondria, basal cell respiration was reduced. Mitochondrial DNA levels appeared normal. However, a higher amount of mitochondrial DNA was present in the cytosol, suggesting a pronounced mitochondrial DNA misplacement which can promote a pro-inflammatory response mediating by cGAS/STING. Thus, this case report further expands the clinical and pathological phenotype of A382T mutation.

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Increased plasma levels of mitochondrial DNA and pro-inflammatory cytokines in patients with progressive multiple sclerosis

Cited by 19 publications

References 27 publications

Mitochondrial DNA and Exercise: Implications for Health and Injuries in Sports

Mitochondrial DNA and Exercise: Implications for Health and Injuries in Sports

Increased Plasma Levels of Mitochondrial DNA and Normal Inflammasome Gene Expression in Monocytes Characterize Patients With Septic Shock Due to Multidrug Resistant Bacteria

Mitochondrial and Endoplasmic Reticulum Alterations in a Case of Amyotrophic Lateral Sclerosis Caused by TDP-43 A382T Mutation

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