Activation of skeletal muscle mitophagy in a murine model of pulmonary and systemic inflammation
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…
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In a murine model of lung injury induced by LPS instillation, transcription of mitophagy-related genes BNIP3L and PARKIN is enhanced and FUNDC1 is decreased.
“The first study was performed in a murine model of lung injury (induced by LPS instillation) and showed an enhanced transcription of mitophagy-related genes such as BNIP3L and PARKIN and a decrease of FUNDC1 [108].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [108]
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Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
Henrot, P., Dupin, I., Schilfarth, P., Esteves, P., Blervaque, L., Zysman, M., Gouzi, F., Hayot, M., Pomiès, P., & Berger, P. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076454 · Cited by 85 · see citing works
“The same authors simultaneously investigated COPD patients’ quadriceps biopsies and found decreased FUNDC1 and PINK1 at the protein level, whereas Parkin was increased.”
Background
- Authors
- Leermakers, P., Remels, A., Langen, R., Schols, A., & Gosker, H.
- Affiliations
- Maastricht University Medical Centre (NL)
- Venue
- 3.1 Molecular Pathology and Functional Genomics
- Publisher
- European Respiratory Society
- Published
- 2016-09
- Pages
- PA3402
- OpenAlex
- W2551764246
- Cited by
- 1
- References
- 0
- Citations by year
- 2023: 1
- Type
- conference abstract
- Language
- en
- Open access
- closed
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitophagy, skeletal muscle, systemic inflammation, lung inflammation, mitochondrial biogenesis, mitochondrial homeostasis, chronic obstructive pulmonary disease, lipopolysaccharide, oxidative phosphorylation, PGC-1α, NRF1, TFAM, BNIP3L, Parkin, FUNDC1, autophagy, gastrocnemius
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