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  1. Article ; Online: Mitochondrial translocation of vitamin D receptor is mediated by the permeability transition pore in human keratinocyte cell line.

    Silvagno, Francesca / Consiglio, Marco / Foglizzo, Valentina / Destefanis, Michele / Pescarmona, Gianpiero

    PloS one

    2013  Volume 8, Issue 1, Page(s) e54716

    Abstract: Background: Vitamin D receptor (VDR) is a well known transcriptional regulator, active as heterodimer in association with coactivators and corepressors. In addition it has been described the extranuclear distribution of the receptor and in particular ... ...

    Abstract Background: Vitamin D receptor (VDR) is a well known transcriptional regulator, active as heterodimer in association with coactivators and corepressors. In addition it has been described the extranuclear distribution of the receptor and in particular the recently reported mitochondrial localization in platelets and megakaryocytes is intriguing because it appears to be a common feature of steroid receptors. Whereas for other members of the steroid receptor family the mitochondrial function has been explored, up to now nothing is known about a mitochondrial form of VDR in human proliferating cells.
    Methodology/principal findings: In this study we characterized for the first time the mitochondrial localization of VDR in the human keratinocyte cell line HaCaT. In proliferating HaCaT cells VDR was abundantly expressed in mitochondria in association with its binding partner RXRα and the import was ligand-independent. By immunoprecipitation studies we demonstrated the interaction of VDR with proteins of the permeability transition pore (PTP), VDAC and StAR. We then adopted different pharmacological and silencing approaches with the aim of hampering PTP function, either affecting PTP opening or abating the expression of the complex member StAR. By all means the impairment of pore function led to a reduction of mitochondrial levels of VDR.
    Conclusions: The results reported here demonstrate a ligand-independent mitochondrial import of VDR through the permeability transition pore, and open interesting new perspectives on PTP function as transporter and on VDR role in mitochondria.
    MeSH term(s) Cell Line ; Humans ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Ligands ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Membrane Transport Proteins/physiology ; Mitochondrial Permeability Transition Pore ; Protein Transport ; Receptors, Calcitriol/metabolism ; Receptors, Calcitriol/physiology ; Retinoid X Receptors/metabolism
    Chemical Substances Ligands ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Receptors, Calcitriol ; Retinoid X Receptors
    Language English
    Publishing date 2013-01-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0054716
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Extremely low frequency electromagnetic fields affect proliferation and mitochondrial activity of human cancer cell lines.

    Destefanis, Michele / Viano, Marta / Leo, Christian / Gervino, Gianpiero / Ponzetto, Antonio / Silvagno, Francesca

    International journal of radiation biology

    2015  Volume 91, Issue 12, Page(s) 964–972

    Abstract: Purpose: To date, the effects of electromagnetic fields on cell metabolism have been overlooked. The objective of the present study was to investigate the influence of extremely low frequency electromagnetic fields (ELF-EMF) over mitochondrial ... ...

    Abstract Purpose: To date, the effects of electromagnetic fields on cell metabolism have been overlooked. The objective of the present study was to investigate the influence of extremely low frequency electromagnetic fields (ELF-EMF) over mitochondrial metabolism and the consequent impact on cancer cell growth.
    Materials and methods: The effects of ELF-EMF on cancer growth were investigated in several human cancer cell lines by crystal violet assay. The modulation of mitochondrial activity was assessed by cytofluorimetric evaluation of membrane potential and by real-time quantification of mitochondrial transcription. Moreover the expression of several mitochondrial proteins and their levels in the organelle were evaluated.
    Results: The long-term exposure to ELF-EMF reduced the proliferation of several cancer cell lines and the effect was associated to an increased mitochondrial activity without evident changes in ATP levels. The results of our experiments excluded a transcriptional modulation of mitochondrial respiratory complexes, rather suggesting that ELF-EMF increased the energy demand. The altered mitochondrial metabolism led to changes in mitochondrial protein profile. In fact we found a downregulated expression of mitochondrial phospho-ERK, p53 and cytochrome c.
    Conclusion: The results of the present study indicate that ELF-EMF can negatively modulate cancer cell growth increasing respiratory activity of cells and altering mitochondrial protein expression.
    MeSH term(s) Cell Count ; Cell Line, Tumor ; Cell Proliferation/radiation effects ; Electromagnetic Fields/adverse effects ; Electron Transport/radiation effects ; Gene Expression Regulation/radiation effects ; Humans ; Membrane Potential, Mitochondrial/radiation effects ; Mitochondria/metabolism ; Mitochondria/radiation effects ; Mitochondrial Proteins/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic/radiation effects
    Chemical Substances Mitochondrial Proteins ; RNA, Messenger
    Language English
    Publishing date 2015
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3065-x
    ISSN 1362-3095 ; 0020-7616 ; 0955-3002
    ISSN (online) 1362-3095
    ISSN 0020-7616 ; 0955-3002
    DOI 10.3109/09553002.2015.1101648
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The vitamin D receptor inhibits the respiratory chain, contributing to the metabolic switch that is essential for cancer cell proliferation.

    Consiglio, Marco / Destefanis, Michele / Morena, Deborah / Foglizzo, Valentina / Forneris, Mattia / Pescarmona, Gianpiero / Silvagno, Francesca

    PloS one

    2014  Volume 9, Issue 12, Page(s) e115816

    Abstract: We recently described the mitochondrial localization and import of the vitamin D receptor (VDR) in actively proliferating HaCaT cells for the first time, but its role in the organelle remains unknown. Many metabolic intermediates that support cell growth ...

    Abstract We recently described the mitochondrial localization and import of the vitamin D receptor (VDR) in actively proliferating HaCaT cells for the first time, but its role in the organelle remains unknown. Many metabolic intermediates that support cell growth are provided by the mitochondria; consequently, the identification of proteins that regulate mitochondrial metabolic pathways is of great interest, and we sought to understand whether VDR may modulate these pathways. We genetically silenced VDR in HaCaT cells and studied the effects on cell growth, mitochondrial metabolism and biosynthetic pathways. VDR knockdown resulted in robust growth inhibition, with accumulation in the G0G1 phase of the cell cycle and decreased accumulation in the M phase. The effects of VDR silencing on proliferation were confirmed in several human cancer cell lines. Decreased VDR expression was consistently observed in two different models of cell differentiation. The impairment of silenced HaCaT cell growth was accompanied by sharp increases in the mitochondrial membrane potential, which sensitized the cells to oxidative stress. We found that transcription of the subunits II and IV of cytochrome c oxidase was significantly increased upon VDR silencing. Accordingly, treatment of HaCaT cells with vitamin D downregulated both subunits, suggesting that VDR may inhibit the respiratory chain and redirect TCA intermediates toward biosynthesis, thus contributing to the metabolic switch that is typical of cancer cells. In order to explore this hypothesis, we examined various acetyl-CoA-dependent biosynthetic pathways, such as the mevalonate pathway (measured as cholesterol biosynthesis and prenylation of small GTPases), and histone acetylation levels; all of these pathways were inhibited by VDR silencing. These data provide evidence of the role of VDR as a gatekeeper of mitochondrial respiratory chain activity and a facilitator of the diversion of acetyl-CoA from the energy-producing TCA cycle toward biosynthetic pathways that are essential for cellular proliferation.
    MeSH term(s) Cell Line, Tumor ; Cell Proliferation ; Cellular Reprogramming ; Electron Transport ; G1 Phase Cell Cycle Checkpoints ; Humans ; M Phase Cell Cycle Checkpoints ; Metabolic Networks and Pathways ; Mitochondria/metabolism ; Neoplasms/metabolism ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism
    Chemical Substances Receptors, Calcitriol
    Language English
    Publishing date 2014-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0115816
    Database MEDical Literature Analysis and Retrieval System OnLINE

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