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  1. Article ; Online: Protocol for the isolation and culture of microglia, astrocytes, and neurons from the same mouse brain.

    Leites, Elvira P / Morais, Vanessa A

    STAR protocols

    2024  Volume 5, Issue 1, Page(s) 102804

    Abstract: Studying the intrinsic properties of microglia, astrocytes, and neurons is essential to our understanding of brain function. Here, we present a protocol to isolate and culture these neural cells from the same mouse brain. Using immunocapture magnetic ... ...

    Abstract Studying the intrinsic properties of microglia, astrocytes, and neurons is essential to our understanding of brain function. Here, we present a protocol to isolate and culture these neural cells from the same mouse brain. Using immunocapture magnetic beads, we describe steps for dissociating, cleaning, and sequentially separating brains from 9-day-old mice into microglia, astrocytes, and neurons. Following these detailed procedures for seeding and culturing of isolated cells, we can address critical questions related to brain function.
    MeSH term(s) Mice ; Animals ; Astrocytes ; Microglia ; Neurons/physiology ; Brain ; Immunomagnetic Separation
    Language English
    Publishing date 2024-01-11
    Publishing country United States
    Document type Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2023.102804
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Protocol for the isolation and culture of microglia, astrocytes, and neurons from the same mouse brain.

    Leites, Elvira P / Morais, Vanessa A

    STAR protocols

    2024  Volume 5, Issue 1, Page(s) 102869

    Language English
    Publishing date 2024-02-01
    Publishing country United States
    Document type Published Erratum
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2024.102869
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Lineage-specific changes in mitochondrial properties during neural stem cell differentiation.

    Soares, Rita / Lourenço, Diogo M / Mota, Isa F / Sebastião, Ana M / Xapelli, Sara / Morais, Vanessa A

    Life science alliance

    2024  Volume 7, Issue 7

    Abstract: Neural stem cells (NSCs) reside in discrete regions of the adult mammalian brain where they can differentiate into neurons, astrocytes, and oligodendrocytes. Several studies suggest that mitochondria have a major role in regulating NSC fate. Here, we ... ...

    Abstract Neural stem cells (NSCs) reside in discrete regions of the adult mammalian brain where they can differentiate into neurons, astrocytes, and oligodendrocytes. Several studies suggest that mitochondria have a major role in regulating NSC fate. Here, we evaluated mitochondrial properties throughout NSC differentiation and in lineage-specific cells. For this, we used the neurosphere assay model to isolate, expand, and differentiate mouse subventricular zone postnatal NSCs. We found that the levels of proteins involved in mitochondrial fusion (Mitofusin [Mfn] 1 and Mfn 2) increased, whereas proteins involved in fission (dynamin-related protein 1 [DRP1]) decreased along differentiation. Importantly, changes in mitochondrial dynamics correlated with distinct patterns of mitochondrial morphology in each lineage. Particularly, we found that the number of branched and unbranched mitochondria increased during astroglial and neuronal differentiation, whereas the area occupied by mitochondrial structures significantly reduced with oligodendrocyte maturation. In addition, comparing the three lineages, neurons revealed to be the most energetically flexible, whereas astrocytes presented the highest ATP content. Our work identified putative mitochondrial targets to enhance lineage-directed differentiation of mouse subventricular zone-derived NSCs.
    MeSH term(s) Animals ; Neural Stem Cells/metabolism ; Neural Stem Cells/cytology ; Mitochondria/metabolism ; Mice ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Astrocytes/metabolism ; Astrocytes/cytology ; Mitochondrial Dynamics ; Oligodendroglia/metabolism ; Oligodendroglia/cytology ; Neurons/metabolism ; Neurons/cytology ; Cells, Cultured ; Mitochondrial Proteins/metabolism ; Mitochondrial Proteins/genetics ; GTP Phosphohydrolases/metabolism ; GTP Phosphohydrolases/genetics ; Neurogenesis ; Lateral Ventricles/cytology ; Lateral Ventricles/metabolism ; Dynamins
    Chemical Substances Mfn1 protein, mouse (EC 3.6.1.-) ; Mfn2 protein, mouse (EC 3.6.1.-) ; Dnm1l protein, mouse (EC 3.6.5.5) ; Mitochondrial Proteins ; GTP Phosphohydrolases (EC 3.6.1.-) ; Dynamins (EC 3.6.5.5)
    Language English
    Publishing date 2024-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202302473
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Reduced penetrance of Parkinson's disease models

    Morais, Vanessa A. / Vos, Melissa

    Medizinische Genetik

    2022  Volume 34, Issue 2, Page(s) 117

    Language German
    Document type Article
    ZDB-ID 1083376-6
    ISSN 0936-5931
    Database Current Contents Medicine

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  5. Article ; Online: Synapses: The Brain's Energy-Demanding Sites.

    Faria-Pereira, Andreia / Morais, Vanessa A

    International journal of molecular sciences

    2022  Volume 23, Issue 7

    Abstract: The brain is one of the most energy-consuming organs in the mammalian body, and synaptic transmission is one of the major contributors. To meet these energetic requirements, the brain primarily uses glucose, which can be metabolized through glycolysis ... ...

    Abstract The brain is one of the most energy-consuming organs in the mammalian body, and synaptic transmission is one of the major contributors. To meet these energetic requirements, the brain primarily uses glucose, which can be metabolized through glycolysis and/or mitochondrial oxidative phosphorylation. The relevance of these two energy production pathways in fulfilling energy at presynaptic terminals has been the subject of recent studies. In this review, we dissect the balance of glycolysis and oxidative phosphorylation to meet synaptic energy demands in both resting and stimulation conditions. Besides ATP output needs, mitochondria at synapse are also important for calcium buffering and regulation of reactive oxygen species. These two mitochondrial-associated pathways, once hampered, impact negatively on neuronal homeostasis and synaptic activity. Therefore, as mitochondria assume a critical role in synaptic homeostasis, it is becoming evident that the synaptic mitochondria population possesses a distinct functional fingerprint compared to other brain mitochondria. Ultimately, dysregulation of synaptic bioenergetics through glycolytic and mitochondrial dysfunctions is increasingly implicated in neurodegenerative disorders, as one of the first hallmarks in several of these diseases are synaptic energy deficits, followed by synapse degeneration.
    MeSH term(s) Animals ; Brain/metabolism ; Energy Metabolism/physiology ; Mammals ; Presynaptic Terminals/metabolism ; Synapses/metabolism ; Synaptic Transmission/physiology
    Language English
    Publishing date 2022-03-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23073627
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: BrainPhys Neuronal Media Support Physiological Function of Mitochondria in Mouse Primary Neuronal Cultures.

    Faria-Pereira, Andreia / Temido-Ferreira, Mariana / Morais, Vanessa A

    Frontiers in molecular neuroscience

    2022  Volume 15, Page(s) 837448

    Abstract: ... In ... ...

    Abstract In vitro
    Language English
    Publishing date 2022-06-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452967-9
    ISSN 1662-5099
    ISSN 1662-5099
    DOI 10.3389/fnmol.2022.837448
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mitochondrial quality control pathways: PINK1 acts as a gatekeeper.

    Leites, Elvira P / Morais, Vanessa A

    Biochemical and biophysical research communications

    2017  Volume 500, Issue 1, Page(s) 45–50

    Abstract: Mitochondria have a pivotal role in the maintenance of cell homeostasis and survival. Mitochondria are involved in processes such as ATP production, reactive oxygen species production, apoptosis induction, calcium homeostasis and protein degradation. ... ...

    Abstract Mitochondria have a pivotal role in the maintenance of cell homeostasis and survival. Mitochondria are involved in processes such as ATP production, reactive oxygen species production, apoptosis induction, calcium homeostasis and protein degradation. Thus, mechanisms that regulate the intrinsic quality of mitochondria have a crucial role in dictating overall cell fate. The importance of these well-regulated mechanisms is highlighted in disease scenarios such as neurodegeneration, cancer and neuromuscular atrophy. How mitochondria senses and regulates their intrinsic quality control, and consequently cell survival, is still not fully understood. In this review, we discuss the pathways that are at present considered as state-of-the-art for mitochondria quality control regulation, and highlight a mitochondrial protein-PINK1-that has revealed to act as a mitochondrial gatekeeper able to sense the presence of healthy or damaged mitochondria.
    MeSH term(s) Apoptosis/genetics ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Gene Expression Regulation ; Homeostasis/genetics ; Humans ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Degradation/genetics ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Muscular Atrophy/genetics ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; rho GTP-Binding Proteins/genetics ; rho GTP-Binding Proteins/metabolism
    Chemical Substances Microtubule-Associated Proteins ; Mitochondrial Proteins ; Reactive Oxygen Species ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27) ; Protein Kinases (EC 2.7.-) ; PTEN-induced putative kinase (EC 2.7.11.1) ; GTP Phosphohydrolases (EC 3.6.1.-) ; MFN2 protein, human (EC 3.6.1.-) ; RHOT1 protein, human (EC 3.6.1.-) ; rho GTP-Binding Proteins (EC 3.6.5.2) ; DNM1L protein, human (EC 3.6.5.5)
    Language English
    Publishing date 2017-06-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2017.06.096
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Local mitochondrial replication in the periphery of neurons requires the eEF1A1 protein and thetranslation of nuclear-encoded proteins.

    Cardanho-Ramos, Carlos / Simões, Rúben Alves / Wang, Yi-Zhi / Faria-Pereira, Andreia / Bomba-Warczak, Ewa / Craessaerts, Katleen / Spinazzi, Marco / Savas, Jeffrey N / Morais, Vanessa A

    iScience

    2024  Volume 27, Issue 4, Page(s) 109136

    Abstract: In neurons, it is commonly assumed that mitochondrial replication only occurs in the cell body, after which the mitochondria must travel to the neuron's periphery. However, while mitochondrial DNA replication has been observed to occur away from the cell ...

    Abstract In neurons, it is commonly assumed that mitochondrial replication only occurs in the cell body, after which the mitochondria must travel to the neuron's periphery. However, while mitochondrial DNA replication has been observed to occur away from the cell body, the specific mechanisms involved remain elusive. Using EdU-labelling in mouse primary neurons, we developed a tool to determine the mitochondrial replication rate. Taking of advantage of microfluidic devices, we confirmed that mitochondrial replication also occurs locally in the periphery of neurons. To achieve this, mitochondria require
    Language English
    Publishing date 2024-02-05
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2024.109136
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: CD4

    Cortes-Figueiredo, Filipe / Asseyer, Susanna / Chien, Claudia / Zimmermann, Hanna G / Ruprecht, Klemens / Schmitz-Hübsch, Tanja / Bellmann-Strobl, Judith / Paul, Friedemann / Morais, Vanessa A

    Scientific reports

    2024  Volume 14, Issue 1, Page(s) 7507

    Abstract: Multiple Sclerosis (MS) is a chronic autoimmune demyelinating disease of the central nervous system (CNS), with a largely unknown etiology, where mitochondrial dysfunction likely contributes to neuroaxonal loss and brain atrophy. Mirroring the CNS, ... ...

    Abstract Multiple Sclerosis (MS) is a chronic autoimmune demyelinating disease of the central nervous system (CNS), with a largely unknown etiology, where mitochondrial dysfunction likely contributes to neuroaxonal loss and brain atrophy. Mirroring the CNS, peripheral immune cells from patients with MS, particularly CD4
    MeSH term(s) Humans ; Multiple Sclerosis/genetics ; T-Lymphocytes ; Cross-Sectional Studies ; Longitudinal Studies ; Retrospective Studies ; Multiple Sclerosis, Relapsing-Remitting/genetics ; Demyelinating Diseases ; DNA, Mitochondrial/genetics ; CD4-Positive T-Lymphocytes ; Genotype
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2024-03-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-024-57592-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Mitochondrial Metabolism Drives Low-density Lipoprotein-induced Breast Cancer Cell Migration.

    Nóbrega-Pereira, Sandrina / Santos, Francisco / Oliveira Santos, Miguel / Serafim, Teresa L / Lopes, Ana Patrícia / Coutinho, Diogo / Carvalho, Filipa S / Domingues, Rosário M / Domingues, Pedro / Bernardes de Jesus, Bruno / Morais, Vanessa A / Dias, Sérgio

    Cancer research communications

    2023  Volume 3, Issue 4, Page(s) 709–724

    Abstract: Most cancer-related deaths are due to metastases. Systemic factors, such as lipid-enriched environments [as low-density lipoprotein (LDL)-cholesterol], favor breast cancer, including triple-negative breast cancer (TNBC) metastasis formation. Mitochondria ...

    Abstract Most cancer-related deaths are due to metastases. Systemic factors, such as lipid-enriched environments [as low-density lipoprotein (LDL)-cholesterol], favor breast cancer, including triple-negative breast cancer (TNBC) metastasis formation. Mitochondria metabolism impacts TNBC invasive behavior but its involvement in a lipid-enriched setting is undisclosed. Here we show that LDL increases lipid droplets, induces CD36 and augments TNBC cells migration and invasion
    Significance: LDL induces breast cancer cell migration that relies on CD36 for mitochondrial metabolism and network remodeling, providing an antimetastatic metabolic strategy.
    MeSH term(s) Humans ; Lipoproteins, LDL/pharmacology ; Triple Negative Breast Neoplasms/metabolism ; Reactive Oxygen Species ; Fatty Acids/pharmacology ; Cell Movement
    Chemical Substances Lipoproteins, LDL ; Reactive Oxygen Species ; Fatty Acids
    Language English
    Publishing date 2023-04-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-22-0394
    Database MEDical Literature Analysis and Retrieval System OnLINE

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