scholarly journals Broad scale proteomic analysis of heat-destabilised symbiosis in the hard coral Acropora millepora

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
K. Petrou ◽  
B. L. Nunn ◽  
M. P. Padula ◽  
D. J. Miller ◽  
D. A. Nielsen
Keyword(s):  
Oxidative Stress ◽  
Elevated Temperature ◽  
Energy Production ◽  
Hard Coral ◽  
Host Proteins ◽  
Acropora Millepora ◽  
Cytoskeletal Regulation ◽  
Lipid Stores ◽  
Broad Scale ◽  
Incremental Increase

AbstractCoral reefs across the globe are threatened by warming oceans. The last few years have seen the worst mass coral bleaching events recorded, with more than one quarter of all reefs irreversibly impacted. Considering the widespread devastation, we need to increase our efforts to understanding the physiological and metabolic shifts underlying the breakdown of this important symbiotic ecosystem. Here, we investigated the proteome (PRIDE accession # PXD011668) of both host and symbionts of the reef-building coral Acropora millepora exposed to ambient (~ 28 °C) and elevated temperature (~ 32 °C for 2 days, following a five-day incremental increase) and explored associated biomolecular changes in the symbiont, with the aim of gaining new insights into the mechanisms underpinning the collapse of the coral symbiosis. We identified 1,230 unique proteins (774 host and 456 symbiont) in the control and thermally stressed corals, of which 107 significantly increased and 125 decreased in abundance under elevated temperature relative to the control. Proteins involved in oxidative stress and proteolysis constituted 29% of the host proteins that increased in abundance, with evidence of impairment to endoplasmic reticulum and cytoskeletal regulation proteins. In the symbiont, we detected a decrease in proteins responsible for photosynthesis and energy production (33% of proteins decreased in abundance), yet minimal signs of oxidative stress or proteolysis. Lipid stores increased > twofold despite reduction in photosynthesis, suggesting reduced translocation of carbon to the host. There were significant changes in proteins related to symbiotic state, including proteins linked to nitrogen metabolism in the host and the V-ATPase (-0.6 fold change) known to control symbiosome acidity. These results highlight key differences in host and symbiont proteomic adjustments under elevated temperature and identify two key proteins directly involved in bilateral nutrient exchange as potential indicators of symbiosis breakdown.

scholarly journals Cardioprotective Effects of PPARβ/δ Activation against Ischemia/Reperfusion Injury in Rat Heart Are Associated with ALDH2 Upregulation, Amelioration of Oxidative Stress and Preservation of Mitochondrial Energy Production

2021 ◽  
Vol 22 (12) ◽  
pp. 6399
Author(s):  
Ioanna Papatheodorou ◽  
Eleftheria Galatou ◽  
Georgios-Dimitrios Panagiotidis ◽  
Táňa Ravingerová ◽  
Antigone Lazou
Keyword(s):  
Oxidative Stress ◽  
Mrna Expression ◽  
Energy Production ◽  
Citrate Synthase ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Uncoupling Protein ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Isocitrate Dehydrogenase 2

Accumulating evidence support the cardioprotective properties of the nuclear receptor peroxisome proliferator activated receptor β/δ (PPARβ/δ); however, the underlying mechanisms are not yet fully elucidated. The aim of the study was to further investigate the mechanisms underlying PPARβ/δ-mediated cardioprotection in the setting of myocardial ischemia/reperfusion (I/R). For this purpose, rats were treated with PPARβ/δ agonist GW0742 and/or antagonist GSK0660 in vivo and hearts were subjected to ex vivo global ischemia followed by reperfusion. PPARβ/δ activation improved left ventricular developed pressure recovery, reduced infarct size (IS) and incidence of reperfusion-induced ventricular arrhythmias while it also up-regulated superoxide dismutase 2, catalase and uncoupling protein 3 resulting in attenuation of oxidative stress as evidenced by the reduction in 4-hydroxy-2-nonenal protein adducts and protein carbonyl formation. PPARβ/δ activation also increased both mRNA expression and enzymatic activity of aldehyde dehydrogenase 2 (ALDH2); inhibition of ALDH2 abrogated the IS limiting effect of PPARβ/δ activation. Furthermore, upregulation of PGC-1α and isocitrate dehydrogenase 2 mRNA expression, increased citrate synthase activity as well as mitochondrial ATP content indicated improvement in mitochondrial content and energy production. These data provide new mechanistic insight into the cardioprotective properties of PPARβ/δ in I/R pointing to ALDH2 as a direct downstream target and suggesting that PPARβ/δ activation alleviates myocardial I/R injury through coordinated stimulation of the antioxidant defense of the heart and preservation of mitochondrial function.

Abstract 276: Angiotensin AT1 Receptor Blockade Reverses Age-Related Changes in Myocardial Energy Metabolism and Increases Mitochondrial Biogenesis

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Peter M Abadir ◽  
Ashwin Akki ◽  
Robert Carey ◽  
Ashish Gupta ◽  
Vadappuram Chacko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Mitochondrial Biogenesis ◽  
Energy Production ◽  
Nuclear Gene ◽  
At1 Receptor ◽  
Resonance Spectroscopy ◽  
Receptor Blockade ◽  
Lv Mass ◽  
Old Mice

Aging and mitochondrial function have been closely linked. We recently reported the identification of a mitochondrial angiotensin system. We hypothesized that angiotensin AT1 receptor blockade would increase energy production and mitochondrial biogenesis and reduce oxidative stress in aging hearts. We used Magnetic resonance spectroscopy to measure cardiac energy metabolism and function in young (20 wks old), aged (150 wks old) mice at baseline and after 4 weeks of losartan (50 mg/kg/day). For mitobiogenesis, qPCR was used to calculate CytB (mitochondrial gene)/GAPDH (nuclear gene) ratio and to measure mito-survival genes Sirt1, Sirt3, Nampt, and PGC-1α. Cardiomyocyte mitochondria from young, aged and treated mice were examined with electron microscopy. The expression of nitrotyrosine was quantified by immunohistochemistry. Older animals hearts (n=9) exhibited increase in LV mass (103±9 mg versus 120±8 mg, young (n=8) versus old (n=9), P<0.002). The mean cardiac PCr/ATP was reduced in older animals (1.5±0.2) than that of young mice (2.0±0.3, P<0.0004). Losartan abolished the LV mass increase in older animals (109±11 mg vs 101±7 mg, young versus old, P<0.1) and improved the impaired energy metabolism of the older hearts increasing the PCr/ATP ratios towards those observed in younger animals (1.94±0.01 vs 1.87±0.4, control versus old, P<0.7). Losartan increased EF in older animals (56±5% vs 63±5%, old versus old treated, P<0.01). Losartan increased mitobiogenesis in the hearts of treated young and old mice (3.8+2.5 folds, P<0.02 and 4.3+ 0.9 folds, P<0.0001). Mito-survival genes in the heart were not increased but PGC-1α was up-regulated by 2.8+1.6-fold, P<0.05 and 7+ 1.9-fold, P<0.001 in young and old treated mice. Electron micrograph analysis revealed that aging was associated with swollen cardiac mitochondria and disrupted cristae, which were reversed by Losartan. Losartan in older animals significantly reduced oxidative damage as evidenced by less Nitrotyrosine staining score in cardiomyocytes (2.5±0.5 vs. 1.3±0.4, old versus old treated, P<0.0009). Our results indicate that Losartan in aging increased mitobiogenesis, reduced oxidative stress, improved energy production and restored cardiac function to the healthy young adult level.

scholarly journals Impaired Mitochondrial Energy Production Causes Light-Induced Photoreceptor Degeneration Independent of Oxidative Stress

PLoS Biology ◽  
2015 ◽  
Vol 13 (7) ◽  
pp. e1002197 ◽  
Author(s):  
Manish Jaiswal ◽  
Nele A. Haelterman ◽  
Hector Sandoval ◽  
Bo Xiong ◽  
Taraka Donti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Production ◽  
Photoreceptor Degeneration ◽  
Mitochondrial Energy Production

scholarly journals Tissue- and cellular-level allocation of autotrophic and heterotrophic nutrients in the coral symbiosis – A NanoSIMS study

2018 ◽  
Author(s):  
Thomas Krueger ◽  
Julia Bodin ◽  
Noa Horwitz ◽  
Céline Loussert-Fonta ◽  
Adrian Sakr ◽  
...  
Keyword(s):  
Elevated Temperature ◽  
Cellular Level ◽  
Nutrient Fluxes ◽  
Stylophora Pistillata ◽  
Feeding Modes ◽  
Brine Shrimps ◽  
Nutrient Partitioning ◽  
Tight Connection ◽  
C And N ◽  
Lipid Stores

AbstractCorals access inorganic seawater nutrients through their autotrophic endosymbiotic dinoflagellates, but also capture planktonic prey through heterotrophic feeding. Correlating NanoSIMS and TEM imaging, we visualize and quantify the subcellular fate of autotrophic and heterotrophic C and N in the coral Stylophora pistillata using stable isotopes. Six scenarios were compared after 6h: autotrophic pulse (13C-bicarbonate, 15N-nitrate) in either unfed or regularly fed corals, and heterotrophic pulse (13C-, 15N-labelled brine shrimps) in regularly fed corals; each at ambient and elevated temperature. Host assimilation of photosynthates was similar under fed and unfed conditions, but symbionts assimilated 10% more C in fed corals. Photoautotrophic C was primarily channelled into host lipid bodies, whereas heterotrophic C and N were generally co-allocated to the tissue. Food-derived label was detected in some subcellular structures associated with the remobilisation of host lipid stores. While heterotrophic input generally exceeded autotrophic input, it was more negatively affected by elevated temperature. The reduced input from both feeding modes at elevated temperature was accompanied by a shift in the partitioning of C and N, benefiting epidermis and symbiont. This study provides a unique view on the nutrient partitioning in corals and highlights the tight connection of nutrient fluxes in symbiotic partners.

192 EXPRESSION OF SELECTED ANTIOXIDANT ENZYMES IN BOVINE OVIDUCT EPITHELIAL CELL (BOEC) IN RESPONSE TO ELEVATED TEMPERATURES IN VITRO

2015 ◽  
Vol 27 (1) ◽  
pp. 187
Author(s):  
L. Rapala ◽  
R. R. Starzynski ◽  
P. Z. Trzeciak ◽  
S. Dabrowski ◽  
A. M. Duszewska
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Antioxidant Enzymes ◽  
Elevated Temperature ◽  
Elevated Temperatures ◽  
Mrna Levels ◽  
Bovine Embryos ◽  
Defence Mechanisms ◽  
Roche Diagnostics

Elevated temperatures have a negative impact on bovine reproduction. One of its effects is an increased concentration of reactive oxygen species (ROS) which may lead to female infertility. Oxidative stress impairs oocyte maturation, fertilization, and embryo development, and it also influences the reproductive tract. One of the defence mechanisms against the increase of ROS is the synthesis of antioxidants. Thus, the aim of this study was to analyse the expression of antioxidant enzymes (superoxide dismutase 1, SOD1; catalase, CAT; and glutathione peroxidase 1, GPX1) in bovine oviduct epithelial cells (BOEC) cultured with or without embryos at elevated temperatures. Ovaries and oviducts were collected from a slaughterhouse. BOECs were mechanically isolated from the oviducts. The oocytes were isolated from ovaries and then maturated and fertilized in vitro. BOEC, after formation of aggregates, were cultured (variant I) in 40-µL droplets of cultured medium (TCM199 25 mM HEPES medium supplemented with 10% FBS, 10 µg mL–1 gentamicin, and 50 µg mL–1 streptomycin) overlaid with mineral oil. Twenty aggregates per droplet were cultured at control (38.5°C) and elevated (41°C) temperatures for 168 h in 5% CO2 in air. Analogously, in variant II, BOEC aggregates were co-cultured with 15 bovine embryos per droplet. Subsequently, the SOD1, CAT, and GPX1 mRNA levels were analysed in BOEC by real-time RT–PCR (Light Cycler, Roche Diagnostics, Warsaw, Poland) and normalized to S18/H2A gene expression. Relative quantification was determined with LightCycler software version 3.5 (Roche Diagnostics) by the second derivative maximum method. Statistical analyses were performed by Portable Statgraphics 5.0 Centurion (Statpoint Technologies Inc., Warrenton, VA). Mean values of SOD1, CAT, and GPX1 expression in BOEC in RT-qPCR analysis were compared using Tukey's HSD test (a = 0.01). Elevated temperature leads to an up-regulation of SOD1 in BOEC cultured (38°C: 0.76 ± 0.12 a.u., n = 44; 41°C: 1.07 ± 0.21 a.u., n = 48) and co-cultured with bovine embryos (38°C: 0.71 ± 0.11 a.u., n = 36; 41°C: 1.04 ± 0.2 a.u., n = 36) and the difference was statistically significant (P < 0.01). The CAT gene expression in BOEC was constant in variant I (38°C: 0.56 ± 0.22 a.u., n = 56; 41°C: 0.58 ± 0.27 a.u., n = 56) and variant II (38°C: 0.48 ± 0.27 a.u., n = 32; 41°C: 0.59 ± 0.29 a.u., n = 24). Also, GPX1 gene expression in BOEC was constant in variant I (38°C: 0.66 ± 0.23 a.u., n = 60; 41°C: 0.61 ± 0.19 a.u., n = 56) and in variant II (38°C: 0.59 ± 0.19 a.u., n = 36; 41°C: 0.64 ± 0.22 a.u., n = 36). In conclusion, elevated temperature leads to an activation of the BOEC's defence mechanisms which are based on SOD1 expression, and which may protect cells against oxidative stress. Elevated temperature doesn't affect the cat and GPX1 expression in BOEC. The presence of embryos does not affect the expression of antioxidant enzymes in BOEC. Research was supported by COST DPN/DWM/MZ/5670/08/09.

scholarly journals Mitophagy and Oxidative Stress in Cancer and Aging: Focus on Sirtuins and Nanomaterials

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Enza Vernucci ◽  
Carlo Tomino ◽  
Francesca Molinari ◽  
Dolores Limongi ◽  
Michele Aventaggiato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Production ◽  
Structural Adjustment ◽  
Molecular Targets ◽  
Production Loss ◽  
Cellular Adaptation ◽  
Invasive Strategy ◽  
Age Related ◽  
New Frontier ◽  
And Oxidative Stress

Mitochondria are the cellular center of energy production and of several important metabolic processes. Mitochondrion health is maintained with a substantial intervention of mitophagy, a process of macroautophagy that degrades selectively dysfunctional and irreversibly damaged organelles. Because of its crucial duty, alteration in mitophagy can cause functional and structural adjustment in the mitochondria, changes in energy production, loss of cellular adaptation, and cell death. In this review, we discuss the dual role that mitophagy plays in cancer and age-related pathologies, as a consequence of oxidative stress, evidencing the triggering stimuli and mechanisms and suggesting the molecular targets for its therapeutic control. Finally, a section has been dedicated to the interplay between mitophagy and therapies using nanoparticles that are the new frontier for a direct and less invasive strategy.

scholarly journals Correction: Impaired Mitochondrial Energy Production Causes Light-Induced Photoreceptor Degeneration Independent of Oxidative Stress

PLoS Biology ◽  
2018 ◽  
Vol 16 (3) ◽  
pp. e1002622 ◽  
Author(s):  
Manish Jaiswal ◽  
Nele A. Haelterman ◽  
Hector Sandoval ◽  
Bo Xiong ◽  
Taraka Donti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Production ◽  
Photoreceptor Degeneration ◽  
Mitochondrial Energy Production
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