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Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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The Inner Mitochondrial Membrane01:28

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The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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Correction: Desai et al. TNFα-Induced Oxidative Stress and Mitochondrial Dysfunction Alter Hypothalamic Neurogenesis and Promote Appetite Versus Satiety Neuropeptide Expression in Mice. <i>Brain Sci.</i><b>2022</b>, <i>12</i>, 900.

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MitoCeption: Transferring Isolated Human MSC Mitochondria to Glioblastoma Stem Cells
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Miro1: new wheels for transferring mitochondria.

Guy Las1, Orian S Shirihai

  • 1Department of Medicine, Boston University School of Medicine, Boston, MA, USA.

The EMBO Journal
|April 9, 2014
PubMed
Summary

Mesenchymal stem cells (MSC) protect damaged cells by transferring mitochondria via tunneling nanotubes (TNT). This transfer is accelerated by Miro1, a protein regulating mitochondrial movement between cells.

Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Stem Cell Therapy

Background:

  • Mesenchymal stem cells (MSC) possess protective capabilities against cellular damage.
  • Mitochondrial damage is implicated in various diseases and aging processes.
  • Intercellular communication via tunneling nanotubes (TNT) facilitates the transfer of cellular components, including mitochondria.

Purpose of the Study:

  • To investigate the mechanisms underlying mitochondrial transfer from MSC to damaged cells.
  • To identify key regulators of mitochondrial transfer through tunneling nanotubes (TNT).
  • To explore the potential of enhancing mitochondrial transfer for therapeutic applications.

Main Methods:

  • Utilized advanced microscopy techniques to visualize mitochondrial transfer between MSC and injured cells.

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  • Investigated the role of specific proteins, including Miro1, in regulating mitochondrial movement.
  • Quantified the impact of Miro1 levels on the efficiency of mitochondrial transfer.

    • Main Results:

    • Mitochondrial transfer via TNT from MSC to damaged cells was confirmed as a protective mechanism.
    • Mitochondrial Rho-GTPase 1 (Miro1) levels were found to be critical for regulating intercellular mitochondrial movement.
    • Increased Miro1 levels significantly accelerated the rate of mitochondrial transfer, enhancing cellular protection.

    Conclusions:

    • Miro1 is the first identified protein that accelerates mitochondrial transfer between cells.
    • Modulating Miro1 levels offers a potential strategy to enhance mitochondrial transfer for therapeutic benefit.
    • Further research into Miro1-mediated mitochondrial transfer could illuminate its role in disease and aging.