CIDEM CMD Phospholipids Trifold 06-26-12

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CIDEM CMD Phospholipids Trifold 06-26-12

Center for Inherited Disorder Services Offered of Energy Metabolism (CIDEM) __________________________________ Wearn Bldg., Room 649 Human Clinical Samples University Hospitals Case Medical Center 11100 Euclid Avenue, Cleveland OH 44106 CIDEM Quantitative Analysis Phospholipid Analysis (including cardiolipin and Tel: 216-844-1286 monolysocardiolipin molecular species) Fax:216-844-8005 Center for Inherited Isolated Skeletal Muscle Mitochondria [email protected] Disorders of Energy Cardiolipin and Monolysocardiolipin Analysis www.case.edu/med/CIDEM/ Skeletal Muscle Metabolism Skin Fibroblasts Tax ID: 34-1720429 CLIA: 36D0680824 ww.case.edu/med/CIDEM Available Fall 2012! CLIA: 36D0925804 Quantitative Analysis NPI: 1578706438 Phospholipid Analysis (including cardiolipin and monolysocardiolipin molecular species) Quantitative Skeletal Muscle (frozen/fresh) Isolated Human Skeletal Muscle Mitochondria Fibroblasts Reference Intervals: Box = Mean ±SD; Whiskers = Range Blood Phospholipid Analysis 300 1.4 ___________________________________ n 250 1.2 by HPLC-MS 1 protei 200 Team Members 0.8 mito 150 Charles Hoppel, MD 0.6 Juhnwan Kim, PhD 100 0.4 Paul Minkler 50 nmol/mg 0.2 0 0 CL PE PC PI PG Quality Control Results for Cardiolipin Center for Mitochondrial Diseases Rat Skeletal Muscle Mitochondria, N = 48, 11% RSD Case Western Reserve University School of Medicine Department of Pharmacology 10900 Euclid Avenue 70 Cleveland, Ohio 44106-4981 60 Center for Mitochondrial Diseases Among the nation’s leading academic medical cen- Case Western Reserve University School of Medicine 50 ters, University Hospitals Case Medical Center is the 40 Department of Pharmacology primary affiliate of Case Western Reserve University 30 10900 Euclid Avenue School of Medicine, a nationally recognized leader in Cleveland, Ohio 44106-4981 20 medical research and education. 10 0 2011/ 07 2012/ 06 Human Skeletal Muscle Mitochondria Human Skin Fibroblasts Human Skeletal Muscle Phospholipid HPLC-MS Chromatogram and Spectra Phospholipid HPLC-MS Chromatogram and Spectra Phospholipid HPLC-MS Chromatogram and Spectra 747.5 766.7 775.7 766.7 766.7 747.6 885.8 788.6 885.8 885.8 599.4 836.5 1452.3 1448.1 1185.7 1163.4 1448.0 786.7 804.7 747.7 1185.7 802.9 802.8 O O OH Symbol Key: O 540.3 O 747.6 O PE - phosphatidylethanolamine monohydroperoxides PG - phosphatidylglycerol Oxidized PI - phosphatidylinositol Cardiolipin O OO H OO H O LPI - lysophosphatidylinositol Reversed- O PS - phosphatidylserine O Phase Ion-Pair dihydroperoxides CL - cardiolipin MLCL - monolysocardiolipin HPLC-MS/MS O O OH O PC - phosphatidylcholine O O OH SM - sphingomyelin O bis monohydroperoxides LPC - lysophosphatidylcholine .

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Cardiolipin and Mitochondrial Cristae Organization
Biochimica et Biophysica Acta 1859 (2017) 1156–1163 Contents lists available at ScienceDirect Biochimica et Biophysica Acta journal homepage: www.elsevier.com/locate/bbamem Cardiolipin and mitochondrial cristae organization Nikita Ikon, Robert O. Ryan ⁎ Children's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609, United States article info abstract Article history: A fundamental question in cell biology, under investigation for over six decades, is the structural organization of Received 23 December 2016 mitochondrial cristae. Long known to harbor electron transport chain proteins, crista membrane integrity is key Received in revised form 3 March 2017 to establishment of the proton gradient that drives oxidative phosphorylation. Visualization of cristae morphol- Accepted 18 March 2017 ogy by electron microscopy/tomography has provided evidence that cristae are tube-like extensions of the mito- Available online 20 March 2017 chondrial inner membrane (IM) that project into the matrix space. Reconciling ultrastructural data with the lipid Keywords: composition of the IM provides support for a continuously curved cylindrical bilayer capped by a dome-shaped Cardiolipin tip. Strain imposed by the degree of curvature is relieved by an asymmetric distribution of phospholipids in Mitochondria monolayer leaﬂets that comprise cristae membranes. The signature mitochondrial lipid, cardiolipin (~18% of Cristae IM phospholipid mass), and phosphatidylethanolamine (34%) segregate to the negatively curved monolayer leaf- Membrane curvature let facing the crista lumen while the opposing, positively curved, matrix-facing monolayer leaﬂet contains pre- Non-bilayer lipid dominantly phosphatidylcholine. Associated with cristae are numerous proteins that function in distinctive Electron transport chain ways to establish and/or maintain their lipid repertoire and structural integrity.
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Serum from Pediatric Dilated Cardiomyopathy Patients Causes Dysregulation of Cardiolipin Biosynthesis and Mitochondrial Function Julie Pires Da Silva, Anastacia M
Serum From Pediatric Dilated Cardiomyopathy Patients Causes Dysregulation of Cardiolipin Biosynthesis and Mitochondrial Function Julie Pires Da Silva, Anastacia M. Garcia, Carissa A. Miyano, Genevieve C. Sparagna, Raleigh Jonscher, Hanan Elajaili, and Carmen C. Sucharov. University of Colorado Anschutz Medical Campus, Aurora, CO Dilated Cardiomyopathy (DCM) Hypothesis - Dilated cardiomyopathy (DCM) is defined as a disorder characterized by Using a novel in vitro model of DCM-related cardiomyocyte remodeling that dilation and impaired contraction of the left ventricle or both ventricles. reproduces the molecular characteristics of pediatric DCM, we hypothesized that the alteration of mitochondrial function in NRVM treated - DCM is the most common form of cardiomyopathy and cause of heart with DCM pediatric sera is associate with changes in cardiolipin content and failure in children older than 1 year of age with an annual incidence of 0.57 mitochondrial β-oxidation pathway. per 100,000 children. - The causes of heart failure (HF) in children differ substantially from those Results found in the adult population and children do not respond well to adult HF therapies. Cardiolipin (CL) - Cardiolipin is a mitochondrial dimeric phospholipid normally located in the inner mitochondrial membrane Figure 5. DCM serum induces significant changes in metabolite levels involved in fatty acid oxidation pathway in NRVMs. A. Heatmap of 41 - CL represent 12-15% of phospholipid mass in heart. In the metabolites differentially expressed in NF and DCM serum-treated NRVMs. n = 4 NF, n= 4 DCM samples, p<0.05. B. Pathway enrichment map analysis heart, 70-80% is (18:2)4CL. of differential metabolites between NF and DCM groups using Figure 3.
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Altered Traffic of Cardiolipin During Apoptosis: Exposure on the Cell Surface As a Trigger for (Antiphospholipid Antibodies)
Hindawi Publishing Corporation Journal of Immunology Research Volume 2015, Article ID 847985, 9 pages http://dx.doi.org/10.1155/2015/847985 Review Article Altered Traffic of Cardiolipin during Apoptosis: Exposure on the Cell Surface as a Trigger for (Antiphospholipid Antibodies) Valeria Manganelli,1 Antonella Capozzi,1 Serena Recalchi,1 Michele Signore,2 Vincenzo Mattei,1,3 Tina Garofalo,1 Roberta Misasi,1 Mauro Degli Esposti,4 and Maurizio Sorice1 1 Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena 324, 00161 Rome, Italy 2Department of Hematology, Oncology and Molecular Medicine, National Institute of Health, Viale Regina Elena 299, 00161 Rome, Italy 3Laboratory of Experimental Medicine and Environmental Pathology, Sabina Universitas, Via dell’Elettronica, 02100 Rieti, Italy 4Italian Institute of Technology, Via Morego 30, 16136 Genoa, Italy Correspondence should be addressed to Maurizio Sorice; [email protected] Received 27 July 2015; Accepted 6 September 2015 Academic Editor: Douglas C. Hooper Copyright © 2015 Valeria Manganelli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Apoptosis has been reported to induce changes in the remodelling of membrane lipids; after death receptor engagement, specific changes of lipid composition occur not only at the plasma membrane, but also in intracellular membranes. This paper focuses on one important aspect of apoptotic changes in cellular lipids, namely, the redistribution of the mitochondria-specific phospholipid, cardiolipin (CL). CL predominantly resides in the inner mitochondrial membrane, even if the rapid remodelling of its acyl chains and the subsequent degradation occur in other membrane organelles.
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Role of Calcium-Independent Phospholipase A2 in the Pathogenesis of Barth Syndrome
Role of calcium-independent phospholipase A2 in the pathogenesis of Barth syndrome Ashim Malhotraa, Irit Edelman-Novemskyb, Yang Xua, Heide Pleskenb, Jinping Mab, Michael Schlamea,b, and Mindong Renb,1 Departments of bCell Biology and aAnesthesiology, New York University Langone Medical Center, New York, NY 10016 Edited by David D. Sabatini, New York University School of Medicine, New York, NY, and approved December 23, 2008 (received for review November 6, 2008) Quantitative and qualitative alterations of mitochondrial cardio- is required for maintaining not only the normal CL fatty acyl lipin have been implicated in the pathogenesis of Barth syndrome, composition, but also normal CL levels. an X-linked cardioskeletal myopathy caused by a deficiency in Although it has been established that tafazzin deficiency tafazzin, an enzyme in the cardiolipin remodeling pathway. We causes both Barth syndrome and a derangement of CL metab- have generated and previously reported a tafazzin-deficient Dro- olism, evidence that it is, in fact, the CL deficiency that con- sophila model of Barth syndrome that is characterized by low tributes to Barth syndrome has been circumstantial (15). To cardiolipin concentration, abnormal cardiolipin fatty acyl compo- elucidate the pathogenic mechanism of Barth syndrome and to sition, abnormal mitochondria, and poor motor function. Here, we identify potential targets for therapeutic intervention, we have first show that tafazzin deficiency in Drosophila disrupts the final created a Drosophila model of Barth syndrome (7) by knocking stage of spermatogenesis, spermatid individualization, and causes out the tafazzin gene and have asked whether the resulting male sterility. This phenotype can be genetically suppressed by phenotypic changes can be suppressed by partially restoring CL inactivation of the gene encoding a calcium-independent phos- homeostasis without correcting the tafazzin defect.
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Antioxidant Synergy of Mitochondrial Phospholipase PNPLA8/Ipla2γ with Fatty Acid–Conducting SLC25 Gene Family Transporters
antioxidants Review Antioxidant Synergy of Mitochondrial Phospholipase PNPLA8/iPLA2γ with Fatty Acid–Conducting SLC25 Gene Family Transporters Martin Jab ˚urek 1,* , Pavla Pr ˚uchová 1, Blanka Holendová 1 , Alexander Galkin 2 and Petr Ježek 1 1 Department of Mitochondrial Physiology, Institute of Physiology of the Czech Academy of Sciences, Vídeˇnská 1084, 14220 Prague, Czech Republic; [email protected] (P.P.); [email protected] (B.H.); [email protected] (P.J.) 2 Department of Pediatrics, Division of Neonatology, Columbia University William Black Building, New York, NY 10032, USA; [email protected] * Correspondence: [email protected]; Tel.: +420-296442789 Abstract: Patatin-like phospholipase domain-containing protein PNPLA8, also termed Ca2+-independent phospholipase A2γ (iPLA2γ), is addressed to the mitochondrial matrix (or peroxisomes), where it may manifest its unique activity to cleave phospholipid side-chains from both sn-1 and sn-2 posi- tions, consequently releasing either saturated or unsaturated fatty acids (FAs), including oxidized FAs. Moreover, iPLA2γ is directly stimulated by H2O2 and, hence, is activated by redox signaling or oxidative stress. This redox activation permits the antioxidant synergy with mitochondrial un- coupling proteins (UCPs) or other SLC25 mitochondrial carrier family members by FA-mediated Citation: Jab ˚urek, M.; Pr ˚uchová,P.; protonophoretic activity, termed mild uncoupling, that leads to diminishing of mitochondrial su- Holendová, B.; Galkin, A.; Ježek, P. peroxide formation. This mechanism allows for the maintenance of the steady-state redox status of Antioxidant Synergy of the cell. Besides the antioxidant role, we review the relations of iPLA2γ to lipid peroxidation since Mitochondrial Phospholipase iPLA2γ is alternatively activated by cardiolipin hydroperoxides and hypothetically by structural γ PNPLA8/iPLA2 with Fatty alterations of lipid bilayer due to lipid peroxidation.
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An Essential Role for Cardiolipin in the Stability and Function of the Mitochondrial Calcium Uniporter
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The Relationship Between Phospholipids and Insulin Resistance: from Clinical to Experimental Studies
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Mathias Haag Dissertation 2010X
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Characterisation of Monolysocardiolipin Acyltransferase Activity
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