Looking Beyond Structure: Membrane Phospholipids of Skeletal Muscle Mitochondria

Heden, Timothy D.; Neufer, P. Darrell; Funai, Katsuhiko

doi:10.1016/j.tem.2016.05.007

Cited by 60 publications

(53 citation statements)

References 82 publications

(93 reference statements)

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“…7 They consist of phosphatidylcholine (PC, 38-45%), phosphatidylethanolamine (PE, 32-39%), cardiolipin (CL, 14-23%), phosphatidylinositol (PI, 2-7%), phosphatidylserine (PS), phosphatidylglycerol (PG), and lyso-phosphatidylcholine (lyso-PC, all less than 3%). 8 These phospholipids not only give rise to the shape of IMM but are also essential for activities of the enzymes of ETS. 8,9 In particular, PE and CL are conical-shaped phospholipids that promote the formation of cristae where ETS enzymes reside.…”

Section: Introductionmentioning

confidence: 99%

“…8 These phospholipids not only give rise to the shape of IMM but are also essential for activities of the enzymes of ETS. 8,9 In particular, PE and CL are conical-shaped phospholipids that promote the formation of cristae where ETS enzymes reside. These non-bilayer lipids lessen torsional strain of the IMM by localizing into the negatively curved inner leaflet.…”

Section: Introductionmentioning

confidence: 99%

“…10 They also bind with high affinity to mitochondrial respiratory complexes and regulate their functions. 8,11 Human mutations that promote loss of mitochondrial PE or CL are detrimental to health. 12-14…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial PE potentiates respiratory enzymes to amplify skeletal muscle aerobic capacity

Heden

Johnson

Ferrara

et al. 2019

Preprint

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41Exercise capacity is a strong predictor of all-cause mortality. Skeletal muscle mitochondrial 42 respiratory capacity, its biggest contributor, adapts robustly to changes in energy demands 43 induced by contractile activity. While transcriptional regulation of mitochondrial enzymes has 44 been extensively studied, there is limited information on how mitochondrial membrane lipids are 45 regulated. Herein, we show that exercise training or muscle disuse alters mitochondrial 46 membrane phospholipids including phosphatidylethanolamine (PE). Addition of PE promoted, 47 whereas removal of PE diminished, mitochondrial respiratory capacity. Surprisingly, skeletal 48 muscle-specific inhibition of mitochondrial-autonomous synthesis of PE caused a respiratory 49 failure due to metabolic insults in the diaphragm muscle. While mitochondrial PE deficiency 50 coincided with increased oxidative stress, neutralization of the latter did not rescue lethality. 51 These findings highlight the previously underappreciated role of mitochondrial membrane 52 phospholipids in dynamically controlling skeletal muscle energetics and function. 53 54 55 157 3B&C), without changes in abundance of ETS enzymes (Figure 3D). PE molecules are bound to 158 ETS complexes I, II, III, and IV, likely facilitating conformational changes and acting as an 159

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mitochondrial PE potentiates respiratory enzymes to amplify skeletal muscle aerobic capacity

Heden

Johnson

Ferrara

et al. 2019

Preprint

Self Cite

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show abstract

“…modulates skeletal muscle mitochondrial function [20]. Genetic studies in mice or humans with defects in coline kinase β, enzyme catalysing the synthesis of PC, demonstrate that reduction of mitochondrial membrane PC content induced enlarged mitochondria, reduced inner membrane potential and caused muscle weakness [20][21][22][23].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

“…Genetic studies in mice or humans with defects in coline kinase β, enzyme catalysing the synthesis of PC, demonstrate that reduction of mitochondrial membrane PC content induced enlarged mitochondria, reduced inner membrane potential and caused muscle weakness [20][21][22][23]. The proper lipid composition of the membranes is crucial for membrane-bound protein machineries to maintain optimal mitochondrial biogenesis and function.…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Myostatin deficiency is associated with lipidomic abnormalities in skeletal muscles

Baati

Feillet‐Coudray

Fouret

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Myostatin (Mstn) deficiency leads to skeletal muscle overgrowth and Mstn inhibition is considered as a promising treatment for muscle-wasting disorders. Mstn gene deletion in mice also causes metabolic changes with decreased mitochondria content, disturbance in mitochondrial respiratory function and increased muscle fatigability. However the impact of MSTN deficiency on these metabolic changes is not fully elucidated. Here, we hypothesized that lack of MSTN will alter skeletal muscle membrane lipid composition in relation with pronounced alterations in muscle function and metabolism. Indeed, phospholipids and in particular cardiolipin mostly present in the inner mitochondrial membrane, play a crucial role in mitochondria function and oxidative phosphorylation process. We observed that Mstn KO muscle had reduced fat membrane transporter levels (FAT/CD36, FABP3, FATP1 and FATP4) associated with decreased lipid oxidative pathway (citrate synthase and β-HAD activities) and impaired lipogenesis (decreased triglyceride and free fatty acid content), indicating a role of mstn in muscle lipid metabolism. We further analyzed phospholipid classes and fatty acid composition by chromatographic methods in muscle and mitochondrial membranes. Mstn KO mice showed increased levels of saturated and polyunsaturated fatty acids at the expense of monounsaturated fatty acids. We also demonstrated, in this phenotype, a reduction in cardiolipin proportion in mitochondrial membrane versus the proportion of others phospholipids, in relation with a decrease in the expression of phosphatidylglycerolphosphate synthase and cardiolipin synthase, enzymes involved in cardiolipin synthesis. These data illustrate the importance of lipids as a link by which MSTN deficiency can impact mitochondrial bioenergetics in skeletal muscle. (Résumé d'auteur

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Epitope Imprinting of Phospholipids by Oriented Assembly at the Oil/Water Interface for the Selective Recognition of Plasma Membranes

et al. 2023

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Phospholipids, as fundamental building blocks of the cell membrane, play important roles for molecule transportation, cell recognition, etc. However, due to the structural diversity and amphipathic nature, there are few methods for the specific recognition of lipids as compared to other biomolecules such as proteins and glycans. Herein, we developed a molecular imprinting strategy for controllable imprinting toward the polar head of phospholipid exposed on the surface of cellular membranes for recognition. Phosphatidylserine, as unique lipid on the outer membrane leaflet of exosome and also hallmark for cell apoptosis, was imprinted with the developed method. The phosphatidylserine imprinted materials showed high efficiency and specific targeting capability not only for apoptotic cell imaging but also for the isolation of exosomes. Collectively, the synthesized molecularly imprinted materials have great potential for selective plasma membrane recognition for targeted drug delivery and biomarker discovery.

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Looking Beyond Structure: Membrane Phospholipids of Skeletal Muscle Mitochondria

Cited by 60 publications

References 82 publications

Mitochondrial PE potentiates respiratory enzymes to amplify skeletal muscle aerobic capacity

Mitochondrial PE potentiates respiratory enzymes to amplify skeletal muscle aerobic capacity

Myostatin deficiency is associated with lipidomic abnormalities in skeletal muscles

Epitope Imprinting of Phospholipids by Oriented Assembly at the Oil/Water Interface for the Selective Recognition of Plasma Membranes

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