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Activation of skeletal muscle mitophagy in a murine model of pulmonary and systemic inflammation

Pieter Leermakers, Alexander Remels, Ramon Langen, Annemie Schols, Harry Gosker
European Respiratory Journal 2016 48: PA3402; DOI: 10.1183/13993003.congress-2016.PA3402
Pieter Leermakers
1NUTRIM, School of Nutrition and Translational Research in Metabolism. Department of Respiratory Medicine, Maastricht University Medical Centre+, Maastricht, LimburgNetherlands
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Alexander Remels
2NUTRIM, School of Nutrition and Translational Research in Metabolism. Department of Pharmacology and Toxicology, Maastricht University Medical Centre+, Maastricht, LimburgNetherlands
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Ramon Langen
1NUTRIM, School of Nutrition and Translational Research in Metabolism. Department of Respiratory Medicine, Maastricht University Medical Centre+, Maastricht, LimburgNetherlands
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Annemie Schols
1NUTRIM, School of Nutrition and Translational Research in Metabolism. Department of Respiratory Medicine, Maastricht University Medical Centre+, Maastricht, LimburgNetherlands
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Harry Gosker
1NUTRIM, School of Nutrition and Translational Research in Metabolism. Department of Respiratory Medicine, Maastricht University Medical Centre+, Maastricht, LimburgNetherlands
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Abstract

Objective: Systemic inflammation has been implicated in skeletal muscle mitochondrial impairment of patients with COPD. Both mitophagy, a selective mitochondrial clearance mechanism, and mitochondrial biogenesis are required for mitochondrial homeostasis. We hypothesized that inflammation-induced loss of muscle mitochondrial capacity is associated with decreased mitochondrial biogenesis and increased mitophagy.

Methods: Mice were subjected to a single intratracheal instillation of lipopolysaccharide (IT-LPS) or NaCl. On several time-points post IT-LPS, muscle (m. gastrocnemius) mitochondrial capacity was assessed by oxidative phosphorylation (OXPHOS) protein levels and citrate synthase (CS) activity. Mitochondrial biogenesis key-regulator protein/mRNA, mitophagy-related protein/mRNA, and autophagy-related mRNA levels were assessed.

Results: Post IT-LPS, OXPHOS protein levels and CS activity were decreased (72h). Moreover, expression levels of key mitochondrial biogenesis regulators were decreased for multiple mRNA targets (48-72h), and PGC-1α (72h) protein, but increased for NRF-1 (72-96h) and TFAM (96h) protein. Autophagy/mitophagy-related mRNA expression was increased for BNIP3L, LC3B, GABARAPL1 (24-48h), and P62 (24-72h). Mitophagy-related protein levels were increased for BNIP3L (24-120h), Parkin (48-120h), or decreased for FUNDC1 (72h).

Conclusion: Systemic inflammation-induced loss of muscle mitochondrial capacity is associated with reduced mitochondrial biogenesis and increased mitophagy-associated protein expression profiles in vivo. Recovery of mitochondrial capacity is associated with mitochondrial biogenesis as well as prolonged mitophagy signaling.

  • Inflammation
  • Peripheral muscle
  • Cell biology
  • Copyright ©the authors 2016
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Activation of skeletal muscle mitophagy in a murine model of pulmonary and systemic inflammation
Pieter Leermakers, Alexander Remels, Ramon Langen, Annemie Schols, Harry Gosker
European Respiratory Journal Sep 2016, 48 (suppl 60) PA3402; DOI: 10.1183/13993003.congress-2016.PA3402

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Activation of skeletal muscle mitophagy in a murine model of pulmonary and systemic inflammation
Pieter Leermakers, Alexander Remels, Ramon Langen, Annemie Schols, Harry Gosker
European Respiratory Journal Sep 2016, 48 (suppl 60) PA3402; DOI: 10.1183/13993003.congress-2016.PA3402
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