The mammalian homologue of yeast Afg1 ATPase (lactation elevated 1) mediates degradation of nuclear-encoded complex IV subunits

Cesnekova, Jana; Rodinová, Marie; Hansı́ková, Hana; Houštěk, J; Zeman, Jiří; Stibůrek, Lukáš

doi:10.1042/bj20151029

Cited by 20 publications

(29 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The molecular mechanism of H 2 S toxicity is mainly the noncompetitive binding of its neutral form to the haem a3/CuB of the binuclear center within the COX I subunit, While it has been proposed that complex IV subunits cannot be the primary target of H 2 S in animals . COX IV is required for normal activity of complexes IV of the respiratory chain and COX IV is crucial for the stability and other subunits assembly of complex IV . In the present study, we have shown that COX I and COX IV expression significantly increase after administration 3 and 5 mg/kg NaHS.…”

Section: Discussionsupporting

confidence: 46%

Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

Feng

Zhang

Shi

et al. 2019

Environmental Toxicology

View full text Add to dashboard Cite

In recent years, the protective effect of hydrogensulfide donor sodium hydrosulfide (NaHS) on multiple organs has been widely reported. The study aimed to explorethe effect of commonly used concentration of NaHS on theliver and its potential damage mechanism. Rats divided into 4 groups: control, NaHS I (1 mg/kg), II (3 mg/kg) and III (5 mg/kg) groups, and each group is divided into four-timepoints (2, 6, 12, and 24 hours). Results showed that H2S concentration increased, mitochondrial complex IV activity inhibited, the COX I and IV subunits and mitochondrial apoptosis pathwayrelated proteins expression increased in atime-and dose-dependent manner. We confirmed that 1 mg/kg NaHS had no injuryeffect on the liver, 3 and 5 mg/kg NaHS inhibitsthe activity of mitochondrial complex IV by promoting COX I and IV subunits expression, leading to the increase in ROS and ultimately inducing apoptosis and liver injury.apoptosis, COX I and COX IV subunits, hepatotoxicity, hydrogen sulfide, reactive oxygen species

show abstract

Section: Discussionsupporting

confidence: 46%

Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

Feng

Zhang

Shi

et al. 2019

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…Also, Lace1, which has been shown to participate in the degradation of Cox4 and Cox6a (Cesnekova et al . ), increased its abundance by more than two‐fold from P1 to P42.…”

Section: Resultsmentioning

confidence: 97%

Protein composition of the muscle mitochondrial reticulum during postnatal development

Kim

Yang

Katti

2019

The Journal of Physiology

View full text Add to dashboard Cite

Key pointsr Muscle mitochondrial networks changed from a longitudinal, fibre parallel orientation to a perpendicular configuration during postnatal development.r Mitochondrial dynamics, mitophagy and calcium uptake proteins were abundant during early postnatal development.r Mitochondrial biogenesis and oxidative phosphorylation proteins were upregulated throughout muscle development.r Postnatal muscle mitochondrial network formation is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.Abstract Striated muscle mitochondria form connected networks capable of rapid cellular energy distribution. However, the mitochondrial reticulum is not formed at birth and the mechanisms driving network development remain unclear. In the present study, we aimed to establish the network formation timecourse and protein expression profile during postnatal development of the murine muscle mitochondrial reticulum. Two-photon microscopy was used to observe mitochondrial network orientation in tibialis anterior (TA) muscles of live mice at postnatal days (P) 1, 7, 14, 21 and 42, respectively. All muscle fibres maintained a longitudinal, fibre parallel mitochondrial network orientation early in development (P1-7). Mixed networks were most common at P14 but, by P21, almost all fibres had developed the perpendicular mitochondrial orientation observed in mature, glycolytic fibres. Tandem mass tag proteomics were then applied to examine changes in 6869 protein abundances in developing TA muscles. Mitochondrial proteins increased by 32% from P1 to P42. In addition, both nuclear-and mitochondrial-DNA encoded oxidative phosphorylation (OxPhos) components were increased during development, whereas OxPhos assembly factors decreased. Although mitochondrial dynamics and mitophagy were induced at P1-7, mitochondrial biogenesis was enhanced after P14. Moreover, calcium signalling Y. Kim and others J Physiol 597.10 proteins and the mitochondrial calcium uniporter had the highest expression early in postnatal development. In conclusion, mitochondrial networks transform from a fibre parallel to perpendicular orientation during the second and third weeks after birth in murine glycolytic skeletal muscle. This structural transition is accompanied by a change in protein expression profile from mitochondria designed for co-ordinated cellular assembly to mitochondria highly specialized for cellular energy metabolism.

show abstract

“…The most enriched GO term from commonly down‐regulated genes in the PDX TA and DIA was mitochondrion ( Figure D). Many of the genes annotating to this category play a role in oxidative phosphorylation including Bcs1l , Rtn4lp1 (Nogo‐interacting mitochondrial protein), and Lace1 ( Figure E) . There were additional repressed genes that annotated to cytosol or membrane that play roles in energy metabolism, including Tfrc (transferrin receptor protein 1), which is a critical regulator iron uptake and Irs1 , which encodes an adapter protein and signal transducer for insulin‐mediated activation of the insulin‐like growth factor 1 receptor.…”

Section: Resultsmentioning

confidence: 99%

Distinct cachexia profiles in response to human pancreatic tumours in mouse limb and respiratory muscle

Nosacka

Delitto

et al. 2020

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

Background Cancer cachexia is a life‐threatening metabolic syndrome that causes significant loss of skeletal muscle mass and significantly increases mortality in cancer patients. Currently, there is an urgent need for better understanding of the molecular pathophysiology of this disease so that effective therapies can be developed. The majority of pre‐clinical studies evaluating skeletal muscle's response to cancer have focused on one or two pre‐clinical models, and almost all have focused specifically on limb muscles. In the current study, we reveal key differences in the histology and transcriptomic signatures of a limb muscle and a respiratory muscle in orthotopic pancreatic cancer patient‐derived xenograft (PDX) mice. Methods To create four cohorts of PDX mice evaluated in this study, tumours resected from four pancreatic ductal adenocarcinoma patients were portioned and attached to the pancreas of immunodeficient NSG mice. Results Body weight, muscle mass, and fat mass were significantly decreased in each PDX line. Histological assessment of cryosections taken from the tibialis anterior (TA) and diaphragm (DIA) revealed differential effects of tumour burden on their morphology. Subsequent genome‐wide microarray analysis on TA and DIA also revealed key differences between their transcriptomes in response to cancer. Genes up‐regulated in the DIA were enriched for extracellular matrix protein‐encoding genes and genes related to the inflammatory response, while down‐regulated genes were enriched for mitochondria related protein‐encoding genes. Conversely, the TA showed up‐regulation of canonical atrophy‐associated pathways such as ubiquitin‐mediated protein degradation and apoptosis, and down‐regulation of genes encoding extracellular matrix proteins. Conclusions These data suggest that distinct biological processes may account for wasting in different skeletal muscles in response to the same tumour burden. Further investigation into these differences will be critical for the future development of effective clinical strategies to counter cancer cachexia.

show abstract

The mammalian homologue of yeast Afg1 ATPase (lactation elevated 1) mediates degradation of nuclear-encoded complex IV subunits

Cited by 20 publications

References 30 publications

Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

Protein composition of the muscle mitochondrial reticulum during postnatal development

Distinct cachexia profiles in response to human pancreatic tumours in mouse limb and respiratory muscle

Contact Info

Product

Resources

About