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New Advances in Mitochondria and Mitochondrial Derived Peptides
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New Advances in Mitochondria and Mitochondrial Derived Peptides

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (29 July 2023) | Viewed by 5947

Special Issue Editor

Dr. Kelvin Yen

E-Mail Website
Guest Editor
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089, USA
Interests: general aging; mitochondrial derived peptides; caloric restriction; neuronal control of feeding behavior and obesity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria and mitochondrial health are central to aging, as they are important in a number of critical processes such as energy generation, reactive oxygen species generation, and apoptosis. Mitochondria dysfunction is also found in many age-related diseases, although whether this is cause or effect has yet to be determined. Recently, a novel class of small peptides encoded by the mitochondrial genome has been discovered, and their roles in biological processes have been emerging. These mitochondrial derived peptides (MDPs) have now been linked to cancer, neuroprotection, cytoprotection, and healthspan. In this issue, we will focus on aging, the mitochondria, and this novel class of MDPs.

Dr. Kelvin Yen
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondria
  • aging
  • mitochondrial derived peptides
  • mitochondrial health
  • mitochondria dysfunction

Published Papers (3 papers)

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Research

18 pages, 3397 KiB  
Article
Oxidized Mitochondrial DNA Engages TLR9 to Activate the NLRP3 Inflammasome in Myelodysplastic Syndromes
by Grace A. Ward, Robert P. Dalton III, Benjamin S. Meyer, Amy F. McLemore, Amy L. Aldrich, Nghi B. Lam, Alexis H. Onimus, Nicole D. Vincelette, Thu Le Trinh, Xianghong Chen, Alexandra R. Calescibetta, Sean M. Christiansen, Hsin-An Hou, Joseph O. Johnson, Kenneth L. Wright, Eric Padron, Erika A. Eksioglu and Alan F. List
Int. J. Mol. Sci. 2023, 24(4), 3896; https://doi.org/10.3390/ijms24043896 - 15 Feb 2023
Cited by 8 | Viewed by 2307
Abstract
Myelodysplastic Syndromes (MDSs) are bone marrow (BM) failure malignancies characterized by constitutive innate immune activation, including NLRP3 inflammasome driven pyroptotic cell death. We recently reported that the danger-associated molecular pattern (DAMP) oxidized mitochondrial DNA (ox-mtDNA) is diagnostically increased in MDS plasma although the [...] Read more.
Myelodysplastic Syndromes (MDSs) are bone marrow (BM) failure malignancies characterized by constitutive innate immune activation, including NLRP3 inflammasome driven pyroptotic cell death. We recently reported that the danger-associated molecular pattern (DAMP) oxidized mitochondrial DNA (ox-mtDNA) is diagnostically increased in MDS plasma although the functional consequences remain poorly defined. We hypothesized that ox-mtDNA is released into the cytosol, upon NLRP3 inflammasome pyroptotic lysis, where it propagates and further enhances the inflammatory cell death feed-forward loop onto healthy tissues. This activation can be mediated via ox-mtDNA engagement of Toll-like receptor 9 (TLR9), an endosomal DNA sensing pattern recognition receptor known to prime and activate the inflammasome propagating the IFN-induced inflammatory response in neighboring healthy hematopoietic stem and progenitor cells (HSPCs), which presents a potentially targetable axis for the reduction in inflammasome activation in MDS. We found that extracellular ox-mtDNA activates the TLR9-MyD88-inflammasome pathway, demonstrated by increased lysosome formation, IRF7 translocation, and interferon-stimulated gene (ISG) production. Extracellular ox-mtDNA also induces TLR9 redistribution in MDS HSPCs to the cell surface. The effects on NLRP3 inflammasome activation were validated by blocking TLR9 activation via chemical inhibition and CRISPR knockout, demonstrating that TLR9 was necessary for ox-mtDNA-mediated inflammasome activation. Conversely, lentiviral overexpression of TLR9 sensitized cells to ox-mtDNA. Lastly, inhibiting TLR9 restored hematopoietic colony formation in MDS BM. We conclude that MDS HSPCs are primed for inflammasome activation via ox-mtDNA released by pyroptotic cells. Blocking the TLR9/ox-mtDNA axis may prove to be a novel therapeutic strategy for MDS. Full article
(This article belongs to the Special Issue New Advances in Mitochondria and Mitochondrial Derived Peptides)
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26 pages, 4273 KiB  
Article
Mitochondrial DNA Deficiency and Supplementation in Sus scrofa Oocytes Influence Transcriptome Profiles in Oocytes and Blastocysts
by Takashi Okada, Stephen McIlfatrick and Justin C. St. John
Int. J. Mol. Sci. 2023, 24(4), 3783; https://doi.org/10.3390/ijms24043783 - 14 Feb 2023
Cited by 3 | Viewed by 1785
Abstract
Mitochondrial DNA (mtDNA) deficiency correlates with poor oocyte quality and fertilisation failure. However, the supplementation of mtDNA deficient oocytes with extra copies of mtDNA improves fertilisation rates and embryo development. The molecular mechanisms associated with oocyte developmental incompetence, and the effects of mtDNA [...] Read more.
Mitochondrial DNA (mtDNA) deficiency correlates with poor oocyte quality and fertilisation failure. However, the supplementation of mtDNA deficient oocytes with extra copies of mtDNA improves fertilisation rates and embryo development. The molecular mechanisms associated with oocyte developmental incompetence, and the effects of mtDNA supplementation on embryo development are largely unknown. We investigated the association between the developmental competence of Sus scrofa oocytes, assessed with Brilliant Cresyl Blue, and transcriptome profiles. We also analysed the effects of mtDNA supplementation on the developmental transition from the oocyte to the blastocyst by longitudinal transcriptome analysis. mtDNA deficient oocytes revealed downregulation of genes associated with RNA metabolism and oxidative phosphorylation, including 56 small nucleolar RNA genes and 13 mtDNA protein coding genes. We also identified the downregulation of a large subset of genes for meiotic and mitotic cell cycle process, suggesting that developmental competence affects the completion of meiosis II and first embryonic cell division. The supplementation of oocytes with mtDNA in combination with fertilisation improves the maintenance of the expression of several key developmental genes and the patterns of parental allele-specific imprinting gene expression in blastocysts. These results suggest associations between mtDNA deficiency and meiotic cell cycle and the developmental effects of mtDNA supplementation on Sus scrofa blastocysts. Full article
(This article belongs to the Special Issue New Advances in Mitochondria and Mitochondrial Derived Peptides)
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12 pages, 1122 KiB  
Article
Pentatricopeptide Protein PTCD2 Regulates COIII Translation in Mitochondria of the HeLa Cell Line
by Maria V. Baleva, Ivan Chicherin, Uliana Piunova, Viktor Zgoda, Maxim V. Patrushev, Sergey Levitskii and Piotr Kamenski
Int. J. Mol. Sci. 2022, 23(22), 14241; https://doi.org/10.3390/ijms232214241 - 17 Nov 2022
Cited by 5 | Viewed by 1335
Abstract
Protein biosynthesis in mitochondria is tightly coupled with assembly of inner membrane complexes and therefore must be coordinated with cytosolic translation of the mRNAs corresponding to the subunits which are encoded in the nucleus. Molecular mechanisms underlying the regulation of mitochondrial translation remain [...] Read more.
Protein biosynthesis in mitochondria is tightly coupled with assembly of inner membrane complexes and therefore must be coordinated with cytosolic translation of the mRNAs corresponding to the subunits which are encoded in the nucleus. Molecular mechanisms underlying the regulation of mitochondrial translation remain unclear despite recent advances in structural biology. Until now, only one translational regulator of protein biosynthesis in mammalian mitochondria is known—protein TACO1, which regulates translation of COI mRNA. Here we describe the function of pentatricopeptide-containing protein PTCD2 as a translational regulator of another mitochondrially encoded subunit of cytochrome c oxidase—COIII in the HeLa cell line. Deletion of the PTCD2 gene leads to significant decrease in COIII translation efficiency and impairment in CIV activity. Additionally, we show that PTCD2 protein is partially co-sedimentates with associated mitochondrial ribosome and associates with mitochondrial ribosome proteins in pull-down assays. These data allow concluding that PTCD2 is a specific translational regulator of COIII which attracts the mRNA to the mitochondrial ribosome. Full article
(This article belongs to the Special Issue New Advances in Mitochondria and Mitochondrial Derived Peptides)
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