Characteristics of the rat cardiac sphingolipid pool in two mitochondrial subpopulations

Monette, Jeffrey S.; Gómez, Luis A.; Moreau, Régis; Bemer, Brett A.; Taylor, Alan; Hagen, Tory M.

doi:10.1016/j.bbrc.2010.06.077

Cited by 18 publications

(21 citation statements)

References 36 publications

(43 reference statements)

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“…In addition, biochemical composition of the two cristae structures may differ in terms of lipid or protein contents, which could ultimately influence structure (108). Indeed, examination of the sphingolipid pool in cardiac SSM and IFM has revealed differences in the content of ceramide, which was higher in the SSM (88).…”

Section: Structural and Functional Differencesmentioning

confidence: 99%

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Hollander

Thapa

Shepherd

2014

American Journal of Physiology-Heart and Circulatory Physiology

133

118

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Section: Structural and Functional Differencesmentioning

confidence: 99%

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Hollander

Thapa

Shepherd

2014

American Journal of Physiology-Heart and Circulatory Physiology

133

118

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“…LC was carried out using a Shimadzu high-pressure LC system (Columbia, MD) with LC elution conditions as described previously ( 18 ). The system was coupled to an Applied Biosystems API 3000 triple quadrupole mass spectrometer with a TurboIon spray source operated with both mass analyzers set at unit resolution in positive mode (LC-MS/MS, Applied Biosystems/MDS Sciex API 3000, Foster City, CA).…”

Section: Brain Tissue Extraction For Dha-pc Analysis By Triple Quadrumentioning

confidence: 99%

Novel function of vitamin E in regulation of zebrafish (Danio rerio) brain lysophospholipids discovered using lipidomics

Choi

Leonard

Kasper

et al. 2015

Journal of Lipid Research

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This article is available online at http://www.jlr.org have used zebrafi sh to characterize the molecular consequences of vitamin E defi ciency because zebrafi sh require dietary ␣ -tocopherol, especially during embryonic development ( 2 ). Zebrafi sh also express the ␣ -tocopherol transfer protein ( ␣ -TTP), which facilitates hepatic ␣ -tocopherol secretion into the circulation in humans ( 3 ), and likely facilitates ␣ -tocopherol delivery from the yolk to the developing zebrafi sh embryo ( 4 ). Importantly, when the ␣ -TTP was knocked down in zebrafi sh embryos by 12-15 h postfertilization, the embryonic brain and eyes failed to form appropriately ( 4 ), indicating that ␣ -tocopherol is necessary for nervous system development. Further, during embryonic growth over 72 h both DHA (22:6) and arachidonic acid (AA) (20:4) decreased at faster rates in vitamin E-defi cient (E Ϫ ) compared with vitamin E-suffi cient (E+) zebrafi sh embryos ( 5 ). Moreover, adequate dietary ascorbic acid was necessary to prevent accelerated ␣ -tocopherol defi ciency and tissue damage ( 5 ).We hypothesized that the devastating effects of severe ␣ -tocopherol defi ciency in zebrafi sh embryos ( 4 ) are a result of depletion and alteration of critical brain lipids. Hypothetically, the brain, which is highly enriched in DHA yet cannot synthesize DHA to meet its needs ( 6 ), is highly susceptible to lipid peroxidation in the ␣ -tocopheroldefi cient state. It has been recognized for decades in humans that vitamin E defi ciency causes a progressive spinocerebellar ataxia ( 7 ). Moreover, Ulatowski et al. ( 8 ) have shown that vitamin E is necessary for preservation of Abstract We hypothesized that brains from vitamin E-defi cient (E ؊ ) zebrafi sh ( Danio rerio ) would undergo increased lipid peroxidation because they contain highly polyunsaturated fatty acids, thus susceptible lipids could be identifi ed. Brains from zebrafi sh fed for 9 months defi ned diets without (E ؊ ) or with (E+) added vitamin E (500 mg RRR -␣ -tocopheryl acetate per kilogram diet) were studied. Using an untargeted approach, 1-hexadecanoyl-2-docosahexaenoyl-sn -glycero-3-phosphocholine [DHA-PC 38:6, PC 16:0/22:6]was the lipid that showed the most signifi cant and greatest fold-differences between groups. DHA-PC concentrations were approximately 1/3 lower in E ؊ (4.3 ± 0.6 mg/g) compared with E+ brains (6.5 ± 0.9 mg/g, mean ± SEM, n = 10 per group, P = 0.04). Using lipidomics, 155 lipids in brain extracts were identifi ed. Only four phospholipids (PLs) were different ( P < 0.05) between groups; they were lower in E ؊ brains and contained DHA with DHA-PC 38:6 at the highest abundances. Moreover, hydroxy-DHA-PC 38:6 was increased in E ؊ brains ( P = 0.0341) supporting the hypothesis of DHA peroxidation. More striking was the depletion in E ؊ brains of nearly 60% of 19 different lysophospholipids (lysoPLs) (combined P = 0.0003), which are critical for membrane PL remodeling. Thus, E ؊ brains contained fewer DHA-PLs, more hydroxy-DHA-PCs, and fewer lysoPLs, suggesting t...

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“…Despite being present in the same cell, SSM and IFM have different respiration rates, metabolic enzyme activities, cristae structure and lipid content [31,34,38,42], and are exposed to different subcellular environments. In recent years it has been shown that the two populations have different susceptibilities to damage in disease [11,27].…”

Section: Introductionmentioning

confidence: 99%

Metabolic adaptation to chronic hypoxia in cardiac mitochondria

et al. 2012

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Chronic hypoxia decreases cardiomyocyte respiration, yet the mitochondrial mechanisms remain largely unknown. We investigated the mitochondrial metabolic pathways and enzymes that were decreased following in vivo hypoxia, and questioned whether hypoxic adaptation was protective for the mitochondria. Wistar rats were housed in hypoxia (7 days acclimatisation and 14 days at 11% oxygen), while control rats were housed in normoxia. Chronic exposure to physiological hypoxia increased haematocrit and cardiac vascular endothelial growth factor, in the absence of weight loss and changes in cardiac mass. In both subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria isolated from hypoxic hearts, state 3 respiration rates with fatty acid were decreased by 17-18%, and with pyruvate were decreased by 29-15%, respectively. State 3 respiration rates with electron transport chain (ETC) substrates were decreased only in hypoxic SSM, not in hypoxic IFM. SSM from hypoxic hearts had decreased activities of ETC complexes I, II and IV, which were associated with decreased reactive oxygen species generation and protection against mitochondrial permeability transition pore (MPTP) opening. In contrast, IFM from hypoxic hearts had decreased activity of the Krebs cycle enzyme, aconitase, which did not modify ROS production or MPTP opening. In conclusion, cardiac mitochondrial respiration was decreased following chronic hypoxia, associated with downregulation of different pathways in the two mitochondrial populations, determined by their subcellular location. Hypoxic adaptation was not deleterious for the mitochondria, in fact, SSM acquired increased protection against oxidative damage under the oxygen-limited conditions.

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Characteristics of the rat cardiac sphingolipid pool in two mitochondrial subpopulations

Cited by 18 publications

References 36 publications

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Novel function of vitamin E in regulation of zebrafish (Danio rerio) brain lysophospholipids discovered using lipidomics

Metabolic adaptation to chronic hypoxia in cardiac mitochondria

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