Mitochondrial Impairments in Peripheral Blood Mononuclear Cells of Multiple Sclerosis Patients

Domínguez-Mozo, María Inmaculada; Nieto, María Celeste García-Frontini García-Frontini; Gómez-Calcerrada, María Isabel; Pérez-Pérez, Silvia; García‐Martínez, Maria Ángel; Villar, Luisa María; Villarrubia, Noelia; Costa‐Frossard, Lucienne; Arroyo, Rafael; Álvarez‐Lafuente, Roberto

doi:10.3390/biology11111633

Cited by 3 publications

(2 citation statements)

References 39 publications

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“…Therefore, mitochondrial impairment and the resultant ciliary dysfunction might contribute to the development of autoimmune diseases. Impaired mitochondrial dysfunction has been demonstrated in patients with multiple sclerosis [125], even in their peripheral blood mononuclear cells [126]. The next two sections illustrate the similarities between LPC cells and TISCs.…”

Section: Mitochondria: Principal Actors Besides Cilia To Maintain Blo...mentioning

confidence: 93%

Ciliated, Mitochondria-Rich Postmitotic Cells are Immune-privileged, and Mimic Immunosuppressive Microenvironment of Tumor-Initiating Stem Cells: From Molecular Anatomy to Molecular Pathway

Behnam,

Fazilaty,

Ghadyani

et al. 2023

Front. Biosci. (Landmark Ed)

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Cancer whose major problems are metastasis, treatment resistance, and recurrence is the leading cause of death worldwide. Tumorinitiating stem cells (TiSCs) are a subset of the tumor population responsible for tumor resistance and relapse. Understanding the characteristics and shared features between tumor-initiating stem cells (TiSCs) and long-lived postmitotic cells may hold a key to better understanding the biology of cancer. Postmitotic cells have exited the cell cycle and are transitioned into a non-dividing and terminally differentiated state with a specialized function within a tissue. Conversely, a cancer cell with TiSC feature can divide and produce a variety of progenies, and is responsible for disease progression, tumor resistance to therapy and immune system and disease relapse. Surprisingly, our comprehensive evaluation of TiSCs suggests common features with long-lived post-mitotic cells. They are similar in structure (primary cilia, high mitochondrial content, and being protected by a barrier), metabolism (autophagy and senescence), and function (immunoescape and/or immune-privileged by a blood barrier). In-depth exploration showed how mitochondrial metabolism contributes to these shared features, including high energy demands arising from ciliary and microtubular functionality, increased metabolic activity, and movement. These findings can assist in decoding the remaining properties which offer insights into the biology of TiSCs, with potential implications for enhancing cancer treatment strategies and patient prognosis.

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Section: Mitochondria: Principal Actors Besides Cilia To Maintain Blo...mentioning

confidence: 93%

Ciliated, Mitochondria-Rich Postmitotic Cells are Immune-privileged, and Mimic Immunosuppressive Microenvironment of Tumor-Initiating Stem Cells: From Molecular Anatomy to Molecular Pathway

Behnam,

Fazilaty,

Ghadyani

et al. 2023

Front. Biosci. (Landmark Ed)

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“…The indirect status of brain mitochondria during MS has been assessed by investigating levels of mitochondrial proteins and gene expression from biofluids in MS patients. For example, peripheral blood mononuclear cells (PBMC)s of MS patients shows impaired mitochondrial redox status and deficient antioxidant capacity ( Gonzalo et al, 2019 ; Dominguez-Mozo et al, 2022 ). Lymphocytes selected by flow cytometry from the PBMC pool of MS patients showed significant decreases in mitochondrial respiratory chain complexes indicating compromised mitochondrial function as compared to normal controls ( Gonzalo et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS

Atkinson,

Osunde,

Tiwari-Woodruff

2023

Front. Neurosci.

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Multiple sclerosis (MS) is a demyelinating, degenerating disorder of the central nervous system (CNS) that is accompanied by mitochondria energy production failure. A loss of myelin paired with a deficit in energy production can contribute to further neurodegeneration and disability in patients in MS. Mitochondria are essential organelles that produce adenosine triphosphate (ATP) via oxidative phosphorylation in all cells in the CNS, including neurons, oligodendrocytes, astrocytes, and immune cells. In the context of demyelinating diseases, mitochondria have been shown to alter their morphology and undergo an initial increase in metabolic demand. This is followed by mitochondrial respiratory chain deficiency and abnormalities in mitochondrial transport that contribute to progressive neurodegeneration and irreversible disability. The current methodologies to study mitochondria are limiting and are capable of providing only a partial snapshot of the true mitochondria activity at a particular timepoint during disease. Mitochondrial functional studies are mostly performed in cell culture or whole brain tissue, which prevents understanding of mitochondrial pathology in distinct cell types in vivo. A true understanding of cell-specific mitochondrial pathophysiology of MS in mouse models is required. Cell-specific mitochondria morphology, mitochondria motility, and ATP production studies in animal models of MS will help us understand the role of mitochondria in the normal and diseased CNS. In this review, we present currently used methods to investigate mitochondria function in MS mouse models and discuss the current advantages and caveats with using each technique. In addition, we present recently developed mitochondria transgenic mouse lines expressing Cre under the control of CNS specific promoters to relate mitochondria to disease in vivo.

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Dual Effect of Carnosine on ROS Formation in Rat Cultured Cortical Astrocytes

Diniz,

Parmeggiani,

Brandão

et al. 2023

Mol Neurobiol

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Mitochondrial Impairments in Peripheral Blood Mononuclear Cells of Multiple Sclerosis Patients

Cited by 3 publications

References 39 publications

Ciliated, Mitochondria-Rich Postmitotic Cells are Immune-privileged, and Mimic Immunosuppressive Microenvironment of Tumor-Initiating Stem Cells: From Molecular Anatomy to Molecular Pathway

Ciliated, Mitochondria-Rich Postmitotic Cells are Immune-privileged, and Mimic Immunosuppressive Microenvironment of Tumor-Initiating Stem Cells: From Molecular Anatomy to Molecular Pathway

The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS

Dual Effect of Carnosine on ROS Formation in Rat Cultured Cortical Astrocytes

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