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Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
13:42

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria

Published on: September 7, 2012

Microcin J25 induces the opening of the mitochondrial transition pore and cytochrome c release through superoxide

María Niklison Chirou1, Augusto Bellomio, Fernando Dupuy

  • 1Departamento de Bioquímica de la Nutrición, Instituto Superior de Investigaciones Biológicas, Instituto de Química Biológica, Dr Bernabe Bloj, San Miguel de Tucumán, Argentina.

The FEBS Journal
|July 12, 2008
PubMed

Insights

Microcin J25, an antimicrobial peptide, triggers mitochondrial pore opening and cytochrome c release by increasing superoxide production and calcium uptake. This process involves a specific sequence of events initiated by microcin J25 binding.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Microcin J25 is a lasso-structure antimicrobial peptide.
  • Antimicrobial peptides can target mitochondria.

Purpose of the Study:

  • To elucidate the mechanism by which Microcin J25 affects mitochondrial function.
  • To determine the sequence of events leading to cell death induced by Microcin J25.

Main Methods:

  • Studies involved assessing mitochondrial permeability transition pore opening.
  • Cytochrome c release was measured.
  • Superoxide anion overproduction and calcium uptake were analyzed.
  • Specific inhibitors (superoxide dismutase, ascorbic acid, ruthenium red, cyclosporin A, Mn2+) were used.

Main Results:

  • Microcin J25 induces mitochondrial permeability transition pore opening.
  • Cytochrome c is released from mitochondria.
  • Superoxide anion overproduction and increased calcium uptake are key mediators.
  • A time-dependent sequence was established: Microcin J25 binding → superoxide overproduction → pore opening → mitochondrial swelling → cytochrome c leakage.

Conclusions:

  • Microcin J25 exerts its antimicrobial effect by targeting mitochondria.
  • The mechanism involves oxidative stress and calcium influx, leading to pore opening and apoptosis-related events.

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