Efficient isolation of pure and functional mitochondria from mouse tissues using automated tissue disruption and enrichment with anti-TOM22 magnetic beads

PLoS One. 2013 Dec 12;8(12):e82392. doi: 10.1371/journal.pone.0082392. eCollection 2013.

Abstract

To better understand molecular mechanisms regulating changes in metabolism, as observed e.g. in diabetes or neuronal disorders, the function of mitochondria needs to be precisely determined. The usual isolation methods such as differential centrifugation result in isolates of highly variable quality and quantity. To fulfill the need of a reproducible isolation method from solid tissues, which is suitable to handle parallel samples simultaneously, we developed a protocol based on anti-TOM22 (translocase of outer mitochondrial membrane 22 homolog) antibody-coupled magnetic beads. To measure oxygen consumption rate in isolated mitochondria from various mouse tissues, a traditional Clark electrode and the high-throughput XF Extracellular Flux Analyzer were used. Furthermore, Western blots, transmission electron microscopic and proteomic studies were performed to analyze the purity and integrity of the mitochondrial preparations. Mitochondrial fractions isolated from liver, brain and skeletal muscle by anti-TOM22 magnetic beads showed oxygen consumption capacities comparable to previously reported values and little contamination with other organelles. The purity and quality of isolated mitochondria using anti-TOM22 magnetic beads was compared to traditional differential centrifugation protocol in liver and the results indicated an obvious advantage of the magnetic beads method compared to the traditional differential centrifugation technique.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Automation
  • Cell Fractionation / methods*
  • Centrifugation
  • Magnetic Phenomena*
  • Mice
  • Microspheres*
  • Mitochondria / metabolism*
  • Mitochondria / ultrastructure
  • Mitochondria, Liver / metabolism
  • Mitochondria, Liver / ultrastructure
  • Mitochondria, Muscle / metabolism
  • Mitochondria, Muscle / ultrastructure
  • Mitochondrial Membrane Transport Proteins / immunology*
  • Organ Specificity*
  • Oxygen Consumption
  • Subcellular Fractions / metabolism

Substances

  • Mitochondrial Membrane Transport Proteins

Grants and funding

This work was supported by the Bundesministerium für Bildung und Forschung (BMBF) within the project NGFNPlus under the grant No. 01GS08174 (NGFN Parkinson) and 01GS0858 (DIGTOP) and the Helmholtz Association (Helmholtz Alliance “MentalHealth in an Ageing Society”) (HelMA HA215) to W.W. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.