Linoleic Acid Increases Prostaglandin E2 Release and Reduces Mitochondrial Respiration and Cell Viability in Human Trophoblast-Like Cells

Shrestha, Nirajan; Cuffe, James; Holland, Olivia J.; Perkins, Anthony V.; McAinch, Andrew J.; Hryciw, Deanne H.

doi:10.33594/000000007

Cited by 22 publications

(9 citation statements)

References 67 publications

(86 reference statements)

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“…In an animal model of heart failure, LA has been shown to improve mitochondrial OXPHOS capacity in cultured rat cardiomyocytes ( Maekawa et al, 2019 ). Albeit being important for mitochondrial membrane integrity, high amounts of LA directly reduced the mitochondrial marker enzyme citrate synthase, as well as routine and maximal mitochondrial respiration in a concentration-dependent manner ( Shrestha et al, 2019 ). Furthermore, an excessive LA dietary intake leads to exacerbated arachidonic acid-derived lipid mediators, such as prostaglandin E 2 (PGE 2 ) and leukotriene B 4 (LTB 4 ) ( Shrestha et al, 2019 ).…”

Section: Changes In Plasma and Mitochondrial Membrane Lipid Composition In Patients With Cirrhosis—interplay Between Lipid Mediators And mentioning

confidence: 99%

“…Albeit being important for mitochondrial membrane integrity, high amounts of LA directly reduced the mitochondrial marker enzyme citrate synthase, as well as routine and maximal mitochondrial respiration in a concentration-dependent manner ( Shrestha et al, 2019 ). Furthermore, an excessive LA dietary intake leads to exacerbated arachidonic acid-derived lipid mediators, such as prostaglandin E 2 (PGE 2 ) and leukotriene B 4 (LTB 4 ) ( Shrestha et al, 2019 ). In fact, this is clinically most relevant as patients with AD cirrhosis present with elevated levels of PGE 2 which suppresses macrophage pro-inflammatory cytokine secretion and bacterial killing, mediated via the prostanoid type E receptor-2 (EP2) ( O’Brien et al, 2014 ).…”

Section: Changes In Plasma and Mitochondrial Membrane Lipid Composition In Patients With Cirrhosis—interplay Between Lipid Mediators And mentioning

confidence: 99%

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Mitochondrial Dysfunction in Advanced Liver Disease: Emerging Concepts

Zhang

López‐Vicario

Duran‐Güell

et al. 2021

Front. Mol. Biosci.

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Mitochondria are entrusted with the challenging task of providing energy through the generation of ATP, the universal cellular currency, thereby being highly flexible to different acute and chronic nutrient demands of the cell. The fact that mitochondrial diseases (genetic disorders caused by mutations in the nuclear or mitochondrial genome) manifest through a remarkable clinical variation of symptoms in affected individuals underlines the far-reaching implications of mitochondrial dysfunction. The study of mitochondrial function in genetic or non-genetic diseases therefore requires a multi-angled approach. Taking into account that the liver is among the organs richest in mitochondria, it stands to reason that in the process of unravelling the pathogenesis of liver-related diseases, researchers give special focus to characterizing mitochondrial function. However, mitochondrial dysfunction is not a uniformly defined term. It can refer to a decline in energy production, increase in reactive oxygen species and so forth. Therefore, any study on mitochondrial dysfunction first needs to define the dysfunction to be investigated. Here, we review the alterations of mitochondrial function in liver cirrhosis with emphasis on acutely decompensated liver cirrhosis and acute-on-chronic liver failure (ACLF), the latter being a form of acute decompensation characterized by a generalized state of systemic hyperinflammation/immunosuppression and high mortality rate. The studies that we discuss were either carried out in liver tissue itself of these patients, or in circulating leukocytes, whose mitochondrial alterations might reflect tissue and organ mitochondrial dysfunction. In addition, we present different methodological approaches that can be of utility to address the diverse aspects of hepatocyte and leukocyte mitochondrial function in liver disease. They include assays to measure metabolic fluxes using the comparatively novel Biolog’s MitoPlates in a 96-well format as well as assessment of mitochondrial respiration by high-resolution respirometry using Oroboros’ O2k-technology and Agilent Seahorse XF technology.

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Section: Changes In Plasma and Mitochondrial Membrane Lipid Composition In Patients With Cirrhosis—interplay Between Lipid Mediators And mentioning

confidence: 99%

Section: Changes In Plasma and Mitochondrial Membrane Lipid Composition In Patients With Cirrhosis—interplay Between Lipid Mediators And mentioning

confidence: 99%

Mitochondrial Dysfunction in Advanced Liver Disease: Emerging Concepts

Zhang

López‐Vicario

Duran‐Güell

et al. 2021

Front. Mol. Biosci.

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“…However, Draycott et al observed that fetal 13C-LA concentrations seem to be influenced by the total amount of FA in the maternal diet, more so than by the n-6 to n-3 ratio, concluding that a higher amount of total FA consumed would favor the placental transport of 13C-LA [114]. In addition, Shrestha et al [14] observed that the exposure to LA increased the expression of the transporters FATP1, FATP4, and FABP5 and decreased that of FABP3 in a culture of cytotrophoblasts, indicating that these proteins could regulate the transport of this PUFA. On the other hand, studies on the placental transport of 13C-LA are controversial, and it is still unclear whether maternal-fetal transfer is affected by obesity.…”

Section: Placental Fatty Acid Transportmentioning

confidence: 99%

“…Of these, n-3 and n-6 long chain PUFA (LCPUFA) are of particular interest because they are an integral part of cell membranes and participate in the synthesis of bioactive molecules that regulate multiple signaling pathways [13]. The supply of essential FA to the fetus will depend entirely on maternal consumption, placental transport and metabolism of FA [14]. Therefore, a balanced diet for pregnant and lactating women must in-clude an appropriate supply of FA.…”

Section: Introductionmentioning

confidence: 99%

Impact of Maternal Obesity on the Metabolism and Bioavailability of Polyunsaturated Fatty Acids during Pregnancy and Breastfeeding

et al. 2020

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Prenatal and postnatal development are closely related to healthy maternal conditions that allow for the provision of all nutritional requirements to the offspring. In this regard, an appropriate supply of fatty acids (FA), mainly n-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA), is crucial to ensure a normal development, because they are an integral part of cell membranes and participate in the synthesis of bioactive molecules that regulate multiple signaling pathways. On the other hand, maternal obesity and excessive gestational weight gain affect FA supply to the fetus and neonate, altering placental nutrient transfer, as well as the production and composition of breast milk during lactation. In this regard, maternal obesity modifies FA profile, resulting in low n-3 and elevated n-6 PUFA levels in maternal and fetal circulation during pregnancy, as well as in breast milk during lactation. These modifications are associated with a pro-inflammatory state and oxidative stress with short and long-term consequences in different organs of the fetus and neonate, including in the liver, brain, skeletal muscle, and adipose tissue. Altogether, these changes confer to the offspring a higher risk of developing obesity and its complications, as well as neuropsychiatric disorders, asthma, and cancer. Considering the consequences of an abnormal FA supply to offspring induced by maternal obesity, we aimed to review the effects of obesity on the metabolism and bioavailability of FA during pregnancy and breastfeeding, with an emphasis on LCPUFA homeostasis.

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“…Except for de novo synthesis and elongation of FA, the utilization of free FA is also a key step in lipid metabolism. FABP5 was found to be involved in the transport of large amounts of intracellular FAs into the nucleus to activate PPARG [28, 29]. Previous study indicated that upregulated FABP5 might contribute to excessive fat deposition in domestic ducks [30].…”

Section: Discussionmentioning

confidence: 99%

Transcriptional insights into key genes and pathways controlling muscle lipid metabolism in broiler chickens

Liu

Cui

et al. 2019

BMC Genomics

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BackgroundIntramuscular fat (IMF) is one of the most important factors positively associated with meat quality. Triglycerides (TGs), as the main component of IMF, play an essential role in muscle lipid metabolism. This transcriptome analysis of pectoralis muscle tissue aimed to identify functional genes and biological pathways likely contributing to the extreme differences in the TG content of broiler chickens.ResultsThe study included Jingxing-Huang broilers that were significantly different in TG content (5.81 mg/g and 2.26 mg/g, p < 0.01) and deposition of cholesterol also showed the same trend. This RNA sequencing analysis was performed on pectoralis muscle samples from the higher TG content group (HTG) and the lower TG content group (LTG) chickens. A total of 1200 differentially expressed genes (DEGs) were identified between two groups, of which 59 DEGs were related to TG and steroid metabolism. The HTG chickens overexpressed numerous genes related to adipogenesis and lipogenesis in pectoralis muscle tissue, including the key genes ADIPOQ, CD36, FABP4, FABP5, LPL, SCD, PLIN1, CIDEC and PPARG, as well as genes related to steroid biosynthesis (DHCR24, LSS, MSMO1, NSDHL and CH25H). Additionally, key pathways related to lipid storage and metabolism (the steroid biosynthesis and peroxisome proliferator activated receptor (PPAR) signaling pathway) may be the key pathways regulating differential lipid deposition between HTG group and LTG group.ConclusionsThis study showed that increased TG deposition accompanying an increase in steroid synthesis in pectoralis muscle tissue. Our findings of changes in gene expression of steroid biosynthesis and PPAR signaling pathway in HTG and LTG chickens provide insight into genetic mechanisms involved in different lipid deposition patterns in pectoralis muscle tissue.

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Linoleic Acid Increases Prostaglandin E2 Release and Reduces Mitochondrial Respiration and Cell Viability in Human Trophoblast-Like Cells

Abstract: This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission.

Cited by 22 publications

References 67 publications

Mitochondrial Dysfunction in Advanced Liver Disease: Emerging Concepts

Mitochondrial Dysfunction in Advanced Liver Disease: Emerging Concepts

Impact of Maternal Obesity on the Metabolism and Bioavailability of Polyunsaturated Fatty Acids during Pregnancy and Breastfeeding

Transcriptional insights into key genes and pathways controlling muscle lipid metabolism in broiler chickens

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