Cell biology of cardiac mitochondrial phospholipids

2004 ◽  
Vol 82 (1) ◽  
pp. 99-112 ◽  
Author(s):  
Grant M Hatch
Keyword(s):  
Cell Biology ◽  
Protein Import ◽  
Significant Proportion ◽  
Phospholipid Metabolism ◽  
Barth Syndrome ◽  
Phospholipid Content ◽  
Mitochondrial Lipid ◽  
Functional Components ◽  
Myocardial Electrical Activity ◽  
Normal Cardiac Function

Phospholipids are important structural and functional components of all biological membranes and define the compartmentation of organelles. Mitochondrial phospholipids comprise a significant proportion of the entire phospholipid content of most eukaroytic cells. In the heart, a tissue rich in mitochondria, the mitochondrial phospholipids provide for diverse roles in the regulation of various mitochondrial processes including apoptosis, electron transport, and mitochondrial lipid and protein import. It is well documented that alteration in the content and fatty acid composition of phospholipids within the heart is linked to alterations in myocardial electrical activity. In addition, reduction in the specific mitochondrial phospholipid cardiolipin is an underlying biochemical cause of Barth Syndrome, a rare and often fatal X-linked genetic disease that is associated with cardiomyopathy. Thus, maintenance of both the content and molecular composition of phospholipids synthesized within the mitochondria is essential for normal cardiac function. This review will focus on the function and regulation of the biosynthesis and resynthesis of mitochondrial phospholipids in the mammalian heart.Key words: phospholipid, metabolism, heart, cardiolipin, mitochondria.

scholarly journals Evaluation of S1PR1/pSTAT3 and S1PR2/FOXP1 Expression in Aggressive, Mature B Cell Lymphomas

2018 ◽  
Author(s):  
Mustafa Al-Kawaaz ◽  
Teresa Sanchez ◽  
Michael J Kluk
Keyword(s):  
B Cell ◽  
Cell Biology ◽  
Significant Proportion ◽  
B Cell Lymphoma ◽  
Cell Types ◽  
B Cell Lymphomas ◽  
Not Otherwise Specified ◽  
Survival Pathways ◽  
Sphingosine 1 Phosphate ◽  
G Protein Coupled

AbstractAggressive, mature B-cell lymphomas represent a heterogeneous group of diseases including Burkitt Lymphoma (BL), High Grade B Cell Lymphomas (HGBL) (eg, Double-Hit B cell lymphomas (HGBL-DH: HGBL with MYC and BCL2 and/or BCL6 translocations)), HGBL, Not Otherwise Specified (HGBL, NOS) and Diffuse Large B Cell Lymphoma. The overlapping morphologic and immunohistochemical features of these lymphomas may pose diagnostic challenges in some cases, and a better understanding of potential diagnostic biomarkers and possible therapeutic targets is needed. Sphingosine 1 Phosphate Receptors (S1PR1-5) represent a family of G-protein coupled receptors that bind the sphingolipid (S1P) and influence migration and survival pathways in a variety of cell types, including lymphocytes. S1PRs are emerging as biomarkers in B cell biology and interaction between S1PR pathways and STAT3 or FOXP1 has been reported, especially in DLBCL. Our aim was to extend the understanding of the S1PR1, STAT3 and S1PR2, FOXP1 expression beyond DLBCL, into additional aggressive, mature B cell lymphomas such as BL, HGBL-DH and HGBL,NOS.Herein, we report that S1PR1 and S1PR2 showed different patterns of expression in mantle zones and follicle centers in reactive lymphoid tissue and, among the lymphomas in this study, Burkitt lymphomas showed a unique pattern of expression compared to HGBL and DLBCL. Additionally, we found that S1PR1 and S1PR2 expression was typically mutually exclusive and were expressed in a low proportion of cases (predominantly HGBL involving extranodal sites). Lastly, FOXP1 was expressed in a high proportion of the various case types and pSTAT3 was detected in a significant proportion of HGBL and DLBCL cases. Taken together, these findings provide further evidence that S1PR1, pSTAT3, S1PR2 and FOXP1 play a role in a subset of aggressive mature B cell lymphomas.

Induction of Ca-independent PLA2 and conservation of plasmalogen polyunsaturated fatty acids in diabetic heart

2000 ◽  
Vol 279 (1) ◽  
pp. E25-E32 ◽  
Author(s):  
Jane McHowat ◽  
Michael H. Creer ◽  
Kristine K. Hicks ◽  
Janet H. Jones ◽  
Raetreal McCrory ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Phospholipid Composition ◽  
Phospholipid Metabolism ◽  
Diabetic Rats ◽  
Phospholipid Content ◽  
Diabetic Patients ◽  
Phospholipid Hydrolysis ◽  
Induced Changes ◽  
Docosahexaenoic Acids

Diabetes-induced changes in phospholipase A2(PLA2) activity have been measured in several tissues but are undefined in diabetic myocardium. We measured ventricular PLA2 activity in control, streptozotocin-induced diabetic, and insulin-treated diabetic rats and characterized myocardial phospholipids to determine whether diabetes altered myocardial phospholipid metabolism. Increased membrane-associated Ca2+-independent PLA2 (iPLA2) activity was observed in diabetes that was selective for arachidonylated phospholipids. Increased iPLA2 activity was accompanied by an increase in choline lysophospholipids. Diabetes was associated with marked alterations in the phospholipid composition of the myocardium, characterized by decreases in esterified arachidonic and docosahexaenoic acids and increases in linoleic acid. The decrease in polyunsaturated fatty acids was confined to diacylphospholipids, whereas the relative amount of these fatty acids in plasmalogens was increased. Diabetes-induced changes in PLA2 activity, lysophospholipid production, and alterations in phospholipid composition were all reversed by insulin treatment of diabetic animals. Diabetes-induced changes in membrane phospholipid content and phospholipid hydrolysis may contribute to some of the alterations in myocardial function that are observed in diabetic patients.

STUDIES IN PHOSPHOLIPID METABOLISM: I. EFFECT OF GUANIDOACETIC ACID AND CHOLINE ON LIVER PHOSPHOLIPIDS

1964 ◽  
Vol 42 (8) ◽  
pp. 1183-1194 ◽  
Author(s):  
J. Blumenstein
Keyword(s):  
Total Phospholipid ◽  
Phospholipid Metabolism ◽  
Phospholipid Content ◽  
Subsequent Reduction ◽  
Total Phospholipid Content

An attempt was made to produce 'forced methylation' and subsequent reduction of lecithin content of livers of rats fed a semipurified diet. The addition of guanidoacetic acid to the diet of the rats did not alter either the total phospholipid extracted from their livers or the liver lecithin content significantly. This constant pattern was observed whether choline was included in the diet or not. However, in animals fed a diet deficient in choline, the ratio of lecithin and cephalin extracted from their livers was altered, although the total phospholipid content remained constant.

scholarly journals LIPID COMPOSITION OF CALLUSES CELL NUCLEI OF PLANTS OF DIFFERENT SYSTEMATIC GROUPS

2018 ◽  
Vol 63 (3) ◽  
pp. 335-338
Author(s):  
V. N. Reshetnikov ◽  
O. V. Chizhik
Keyword(s):  
Comparative Analysis ◽  
Cell Cultures ◽  
Metabolic Activity ◽  
Lipid Composition ◽  
Cell Biology ◽  
Neutral Lipids ◽  
Phospholipid Content ◽  
Winter Rye ◽  
Cell Nuclei ◽  
Active Proliferation

The study revealed the results of the comparative analysis of the deoxyribonucleoproteid complex (chromatin) lipid composition in the callus and explant nuclei of plants, belonging to different systematic groups (winter rye, potatoes, peas). It provided the data on the phospho- and neutral lipid composition of the investigated plants and showed that the phospholipid content in the explants from dormant winter rye seed embryos and potato stems, having low metabolic activity, is significantly higher than in the calluses in the stage of active proliferation. Both winter rye and potato calluses tend to have a lower share of neutral lipids, including sterols, in their composition. The revealed factors can be used as markers of metabolic activity of the plant cell biology objects (callus and cell cultures). 

scholarly journals Mitochondrial regulation of ferroptosis

2021 ◽  
Vol 220 (9) ◽  
Author(s):  
Boyi Gan
Keyword(s):  
Cell Death ◽  
Cell Biology ◽  
Lipid Peroxides ◽  
Disease Treatment ◽  
Mitochondrial Regulation ◽  
Defense Systems ◽  
Regulated Cell Death ◽  
Mitochondrial Lipid ◽  
Mitochondria Functions ◽  
New Evidence

Ferroptosis is a form of iron-dependent regulated cell death driven by uncontrolled lipid peroxidation. Mitochondria are double-membrane organelles that have essential roles in energy production, cellular metabolism, and cell death regulation. However, their role in ferroptosis has been unclear and somewhat controversial. In this Perspective, I summarize the diverse metabolic processes in mitochondria that actively drive ferroptosis, discuss recently discovered mitochondria-localized defense systems that detoxify mitochondrial lipid peroxides and protect against ferroptosis, present new evidence for the roles of mitochondria in regulating ferroptosis, and outline outstanding questions on this fascinating topic for future investigations. An in-depth understanding of mitochondria functions in ferroptosis will have important implications for both fundamental cell biology and disease treatment.

Protein import into chloroplasts: an ever-evolving storyThis review is one of a selection of papers published in the Special Issue on Plant Cell Biology.

2006 ◽  
Vol 84 (4) ◽  
pp. 531-542 ◽  
Author(s):  
Matthew D. Smith
Keyword(s):  
Plant Growth ◽  
Cell Biology ◽  
Growth And Development ◽  
Protein Import ◽  
Special Issue ◽  
Plant Growth And Development ◽  
Core Components ◽  
Envelope Membranes ◽  
Inner Envelope ◽  
Selection Of

Chloroplasts are but one type of a diverse group of essential organelles that distinguish plant cells and house many critical biochemical pathways, including photosynthesis. The biogenesis of plastids is essential to plant growth and development and relies on the targeting and import of thousands of nuclear-encoded proteins from the cytoplasm. The import of the vast majority of these proteins is dependent on translocons located in the outer and inner envelope membranes of the chloroplast, termed the Toc and Tic complexes, respectively. The core components of the Toc and Tic complexes have been identified within the last 12 years; however, the precise functions of many components are still being elucidated, and new components are still being identified. In Arabidopsis thaliana (and other species), many of the components are encoded by more than one gene, and it appears that the isoforms differentially associate with structurally distinct import complexes. Furthermore, it appears that these complexes represent functionally distinct targeting pathways, and the regulation of import by these separate pathways may play a role in the differentiation and specific functions of distinct plastid types during plant growth and development. This review summarizes these recent discoveries and emphasizes the mechanisms of differential Toc complex assembly and substrate recognition.

Impaired surfactant phospholipid metabolism in hyperoxic mouse lungs

1981 ◽  
Vol 51 (5) ◽  
pp. 1198-1203 ◽  
Author(s):  
N. J. Gross ◽  
D. M. Smith
Keyword(s):  
Mechanical Properties ◽  
Phospholipid Metabolism ◽  
Phospholipid Content ◽  
In Vitro Synthesis ◽  
Phospholipid Classes ◽  
Surfactant Phospholipids ◽  
Mouse Lungs ◽  
Alveolar Surface

We studied the effect of 98% O2 on the amounts of and in vivo and in vitro synthesis rates of lung phospholipids in the mouse. The alveolar fluid obtained by multiple endobronchial lavages showed a decline in the amounts of all phospholipids between 48 and 72 h. The proportion of phosphatidylcholine that was disaturated did not change up to 96 h. Smaller decreases in phosphatidylcholine of the lung tissue were found at the same times. Between 48 and 72 h the turnover of total and disaturated phosphatidylcholine was greatly decreased, and transit time for both from lung to alveolar fluid was prolonged. At 60 h in vitro incorporation by lung slices of both glycerol and palmitate into disaturated phospholipids was reduced by approximately half, the distribution of label into various phospholipid classes being unchanged. We interpret these data as supporting the hypothesis that hyperoxia impairs the synthesis of surfactant phospholipids in the lung and their transport to the alveolar surface, and that this results in a decrease in the phospholipid content of the alveolar lining layer. These effects could account for altered pulmonary mechanical properties and contribute to the morbidity and mortality of O2 toxicity.

scholarly journals Mechanisms and Alterations of Cardiac Ion Channels Leading to Disease: Role of Ankyrin-B in Cardiac Function

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 211 ◽  
Author(s):  
Holly C. Sucharski ◽  
Emma K. Dudley ◽  
Caullin B.R. Keith ◽  
Mona El Refaey ◽  
Sara N. Koenig ◽  
...  
Keyword(s):  
Ion Channels ◽  
Cardiac Function ◽  
Cell Biology ◽  
Sinus Node ◽  
Conduction Block ◽  
Cardiac Ion Channels ◽  
Life Threatening ◽  
Ankyrin B ◽  
Normal Cardiac Function

Ankyrin-B (encoded by ANK2), originally identified as a key cytoskeletal-associated protein in the brain, is highly expressed in the heart and plays critical roles in cardiac physiology and cell biology. In the heart, ankyrin-B plays key roles in the targeting and localization of key ion channels and transporters, structural proteins, and signaling molecules. The role of ankyrin-B in normal cardiac function is illustrated in animal models lacking ankyrin-B expression, which display significant electrical and structural phenotypes and life-threatening arrhythmias. Further, ankyrin-B dysfunction has been associated with cardiac phenotypes in humans (now referred to as “ankyrin-B syndrome”) including sinus node dysfunction, heart rate variability, atrial fibrillation, conduction block, arrhythmogenic cardiomyopathy, structural remodeling, and sudden cardiac death. Here, we review the diverse roles of ankyrin-B in the vertebrate heart with a significant focus on ankyrin-B-linked cell- and molecular-pathways and disease.

Changes in phospholipid metabolism dependent on calcium-regulated myoblast fusion

1988 ◽  
Vol 66 (10) ◽  
pp. 1110-1118 ◽  
Author(s):  
Victor S. Sauro ◽  
Gregory A. Brown ◽  
Michael R. Hamilton ◽  
Craig K. Strickland ◽  
Kenneth P. Strickland
Keyword(s):  
Calcium Content ◽  
Phospholipid Metabolism ◽  
Myoblast Fusion ◽  
Myoblast Differentiation ◽  
Phospholipid Content ◽  
Phospholipid Synthesis ◽  
Normal Medium ◽  
Low Calcium ◽  
High Calcium ◽  
Fusion Competent Myoblasts

Fusion-competent myoblasts can be prevented from fusing (differentiating) by reducing medium calcium concentrations from 1.65 mM to less than 50 μM. Fusion is completely retarded after 24 h but is noticeable after 48 h and significant after 72 h in low-calcium medium. After 24 h in low-calcium medium, a rapid, synchronous fusion can be initiated by return to normal (high-calcium) medium. Calcium content increases over threefold during myoblast differentiation and closely parallels the fusion process. Phospholipid content is also dependent upon the state of differentiation. Myotubes (fused myoblasts) have an almost twofold greater content of lipid phosphate per milligram of protein compared with that of myoblasts; this increase is localized to increased contents of phosphatidylcholine and pooled phosphatidylinositol – phosphatidylserine. Phospholipid synthesis (32Pi incorporation) is markedly stimulated four- to five-fold when myoblasts grown in low-calcium medium are switched to normal medium. These significant increases are observed in all the major phospholipids studied, predominantly in phosphatidylcholine and pooled phosphatidylinositol – phosphatidylserine, and most noticeably in phosphatidylinositol 4,5-bisphosphate. Furthermore, we show that phosphatidylinositol 4,5-bisphosphate prelabelled with myo-[2-3H]inositol is rapidly degraded after switching from low-calcium medium to normal medium. These changes are not observed in myotubes treated similarly, which suggests that the changes in phospholipid metabolism may be fusion related. These results support a proposal by another author, which suggests that phosphatidylinositol 4,5-bisphosphate breakdown may play an important regulating role in myoblast differentiation.

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