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Bioactive Lipids for Health Benefits

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 13545

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Guest Editor
Department of Clinical Sciences, Section of Biochemistry, Biology and Physics, Università Politecnica delle Marche, 60131 Ancona, Italy
Interests: nitric oxide and its metabolism; oxidative stress; diabetes; obesity; eating disorders; neurodegenerative diseases; infertility; functional food; taste sensitivity
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Special Issue Information

Dear Colleagues,

International Journal of Molecular Sciences (ISSN 1422-0067, IF 4.556) is currently running a Special Issue focused on "Bioactive Lipids for Health Benefits". Dr. Arianna Vignini is serving as Guest Editors for this issue. Based on your excellent expertise, we would be thrilled if you could submit a paper to this issue.

Bioactive lipids are lipids involved in signaling in every cell of every organism. Over the past two decades, they have become increasingly important in many areas of biology. They are the main diffusion mediators of the inflammatory response in tissues and regulate the polarity of cell membranes; As particularly prominent signaling molecules in the immune system, various bioactive lipids are required for the proper functioning of both the innate and adaptive immune system, in the vesicle traffic required to deliver many proteins to the appropriate organelles and to maintain structure and order within the cell. Currently, over thousands of bioactive lipids, including fatty acids and their metabolic products, acylglycerol derivatives, endocannabinoids, lysophospholipids, sphingolipids, cholesterol metabolites, etc., and sterols, sphingolipids have numerous functions important for homeostatic regulation and disease pathologies, such as metabolic diseases, cancer, heart disease, neurodegenerative disorders, obesity, and diabetes.

In this Special Issue, original research and review articles focused on in the field and, specifically, the molecular mechanism of the bioactive lipids participating energy in homeostasis and related disorders, identifying receptors, and exploring the signal transduction of the bioactive lipids, are warmly welcome.

Dr. Arianna Vignini
Guest Editor

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Published Papers (6 papers)

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Research

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14 pages, 2283 KiB  
Article
A Dietary Oxysterol, 7-Ketocholesterol, Exacerbates Imiquimod-Induced Psoriasis-like Dermatitis in Steatohepatitic Mice
by Ayami Saga, Masahiro Koseki, Kotaro Kanno, Jiuyang Chang, Tomoaki Higo, Daisuke Okuzaki, Takeshi Okada, Hiroyasu Inui, Masumi Asaji, Katsunao Tanaka, Takashi Omatsu, Sae Nishihara, Yinghong Zhu, Kaori Ito, Hiroaki Hattori, Ikuyo Ichi, Yoshihiro Kamada, Masafumi Ono, Toshiji Saibara, Tohru Ohama, Shungo Hikoso, Makoto Nishida, Shizuya Yamashita and Yasushi Sakataadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2022, 23(24), 15855; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415855 - 13 Dec 2022
Cited by 3 | Viewed by 1745
Abstract
Patients with psoriasis are at a higher risk of developing nonalcoholic fatty liver disease. We previously identified an oxidized derivative of cholesterol, 7-ketocholesterol (7KC), in diet-induced steatohepatitic mice. Here, we investigated whether 7KC exacerbates psoriasis-like dermatitis by accelerating steatohepatitis in mice. A high-fat/high-cholesterol/high-sucrose/bile [...] Read more.
Patients with psoriasis are at a higher risk of developing nonalcoholic fatty liver disease. We previously identified an oxidized derivative of cholesterol, 7-ketocholesterol (7KC), in diet-induced steatohepatitic mice. Here, we investigated whether 7KC exacerbates psoriasis-like dermatitis by accelerating steatohepatitis in mice. A high-fat/high-cholesterol/high-sucrose/bile salt diet (nonalcoholic steatohepatitis (NASH) diet) with or without 0.0125% 7KC was fed to C57BL/6 mice (7KC or control group) for three weeks to induce steatohepatitis. A 5% imiquimod cream was then applied to the ears and dorsal skin for four days to induce psoriasis-like dermatitis. Hepatic lipid accumulation and inflammatory cell infiltration were exacerbated in the 7KC group compared with the control group after three weeks. Serum tumor necrosis factor-α (TNF-α) levels were also elevated in the 7KC group (108.5 ± 9.8 vs. 83.1 ± 13.1 pg/mL, p < 0.005). Imiquimod cream increased the psoriasis area severity index (PASI) score in mice in the 7KC group (9.14 ± 0.75 vs. 5.17 ± 1.17, p < 0.0001). Additionally, Tnfa, Il23a, Il17a, and Il22 mRNA levels in the dorsal lesion were significantly upregulated. Finally, Th17 cell differentiation and the TNF signaling pathway were enhanced in the dorsal lesions and liver of mice in the 7KC group. These data suggest that steatohepatitis and psoriasis are linked by a potent, diet-related factor. Full article
(This article belongs to the Special Issue Bioactive Lipids for Health Benefits)
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18 pages, 2002 KiB  
Article
Hop Extract Anti-Inflammatory Effect on Human Chondrocytes Is Potentiated When Encapsulated in Rapeseed Lecithin Nanoliposomes
by Émilie Velot, Florent Ducrocq, Loïc Girardeau, Alain Hehn, Séverine Piutti, Cyril Kahn, Michel Linder, Arnaud Bianchi and Elmira Arab-Tehrany
Int. J. Mol. Sci. 2022, 23(20), 12423; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012423 - 17 Oct 2022
Cited by 1 | Viewed by 1511
Abstract
Hop (Humulus lupulus L.) is a plant used as an ingredient in beer or employed for its anti-inflammatory properties. The cultivation of hops is currently dedicated to the brewing industry, where mainly female flowers are used, whereas aerial parts, such as leaves, [...] Read more.
Hop (Humulus lupulus L.) is a plant used as an ingredient in beer or employed for its anti-inflammatory properties. The cultivation of hops is currently dedicated to the brewing industry, where mainly female flowers are used, whereas aerial parts, such as leaves, are considered coproducts. Osteoarthritis is the most common musculoskeletal disease associated with low-grade cartilage inflammation. Liposomes have been shown to be promising systems for drug delivery to cartilage cells, called chondrocytes. The aim of our work was to vectorize hop extract valorized from coproducts as a therapeutic agent to alleviate inflammation in human chondrocytes in vitro. Liquid chromatography allowed the identification of oxidized bitter acids in a methanolic extract obtained from the leaves of Cascade hops. The extract was encapsulated in rapeseed lecithin nanoliposomes, and the physicochemical properties of empty or loaded nanoliposomes exhibited no difference. Increasing concentrations of the hop extract alone, empty nanoliposomes, and loaded nanoliposomes were tested on human chondrocytes to assess biocompatibility. The appropriate conditions were applied to chondrocytes stimulated with interleukin-1β to evaluate their effect on inflammation. The results reveal that encapsulation potentiates the hop extract anti-inflammatory effect and that it might be able to improve joint inflammation in osteoarthritis. Furthermore, these results also show that a “zero waste” chain is something that can be achieved in hop cultivation. Full article
(This article belongs to the Special Issue Bioactive Lipids for Health Benefits)
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14 pages, 2576 KiB  
Article
Linoleic Acid Upregulates Microrna-494 to Induce Quiescence in Colorectal Cancer
by Ruiko Ogata, Shiori Mori, Shingo Kishi, Rika Sasaki, Naoya Iwata, Hitoshi Ohmori, Takamitsu Sasaki, Yukiko Nishiguchi, Chie Nakashima, Kei Goto, Isao Kawahara, Rina Fujiwara-Tani and Hiroki Kuniyasu
Int. J. Mol. Sci. 2022, 23(1), 225; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010225 - 25 Dec 2021
Cited by 13 | Viewed by 2950
Abstract
Cancer dormancy is a state characterized by the quiescence of disseminated cancer cells, and tumor recurrence occurs when such cells re-proliferate after a long incubation period. These cancer cells tend to be treatment resistant and one of the barriers to successful therapeutic intervention. [...] Read more.
Cancer dormancy is a state characterized by the quiescence of disseminated cancer cells, and tumor recurrence occurs when such cells re-proliferate after a long incubation period. These cancer cells tend to be treatment resistant and one of the barriers to successful therapeutic intervention. We have previously reported that long-term treatment of cancer cells with linoleic acid (LA) induces a dormancy-like phenotype. However, the mechanism underpinning this effect has not yet been clarified. Here, we investigate the mechanism of LA-induced quiescence in cancer cells. We first confirmed that long-term treatment of the mouse colorectal cancer cell line CT26 with LA induced quiescence. When these cells were inoculated subcutaneously into a syngeneic mouse and fed with an LA diet, the inoculated cancer cells maintained the quiescent state and exhibited markers of dormancy. LA-treated CT26 cells showed reduced oxidative phosphorylation, glycolysis, and energy production as well as reduced expression of the regulatory factors Pgc1α and MycC. MicroRNA expression profiling revealed that LA induced an upregulation in miR-494. The expression of Pgc1α and MycC were both induced by an miR-494 mimic, and the LA-induced decrease in gene expression was abrogated by an miR-494 inhibitor. The expression of miR-494 was enhanced by the mitochondrial oxidative stress produced by LA. In a syngeneic mouse subcutaneous tumor model, growth suppression by an LA diet and growth delay by LA pretreatment + LA diet were found to have similar effects as administration of an miR-494 mimic. In contrast, the effects of LA were abrogated by an miR-494 inhibitor. Analysis of human colorectal cancer tissue revealed that miR-494 was present at low levels in non-metastatic cases and cases with simultaneous liver metastases but was expressed at high levels in cases with delayed liver metastases, which also exhibited reduced expression of PGC1α and MYCC. These results suggest that miR-494 is involved in cancer dormancy induced by high levels of LA intake and that this microRNA may be valuable in targeting dormant cancer cells. Full article
(This article belongs to the Special Issue Bioactive Lipids for Health Benefits)
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33 pages, 5895 KiB  
Article
Palm Oil-Rich Diet Affects Murine Liver Proteome and S-Palmitoylome
by Ewelina Ziemlińska, Justyna Sobocińska, Anna Świątkowska, Aneta Hromada-Judycka, Gabriela Traczyk, Agata Malinowska, Bianka Świderska, Anna Mietelska-Porowska, Anna Ciesielska and Katarzyna Kwiatkowska
Int. J. Mol. Sci. 2021, 22(23), 13094; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222313094 - 03 Dec 2021
Cited by 6 | Viewed by 2742
Abstract
Palmitic acid (C16:0) is the most abundant saturated fatty acid in animals serving as a substrate in synthesis and β-oxidation of other lipids, and in the modification of proteins called palmitoylation. The influence of dietary palmitic acid on protein S-palmitoylation remains largely [...] Read more.
Palmitic acid (C16:0) is the most abundant saturated fatty acid in animals serving as a substrate in synthesis and β-oxidation of other lipids, and in the modification of proteins called palmitoylation. The influence of dietary palmitic acid on protein S-palmitoylation remains largely unknown. In this study we performed high-throughput proteomic analyses of a membrane-enriched fraction of murine liver to examine the influence of a palm oil-rich diet (HPD) on S-palmitoylation of proteins. HPD feeding for 4 weeks led to an accumulation of C16:0 and C18:1 fatty acids in livers which disappeared after 12-week feeding, in contrast to an accumulation of C16:0 in peritoneal macrophages. Parallel proteomic studies revealed that HPD feeding induced a sequence of changes of the level and/or S-palmitoylation of diverse liver proteins involved in fatty acid, cholesterol and amino acid metabolism, hemostasis, and neutrophil degranulation. The HPD diet did not lead to liver damage, however, it caused progressing obesity, hypercholesterolemia and hyperglycemia. We conclude that the relatively mild negative impact of such diet on liver functioning can be attributed to a lower bioavailability of palm oil-derived C16:0 vs. that of C18:1 and the efficiency of mechanisms preventing liver injury, possibly including dynamic protein S-palmitoylation. Full article
(This article belongs to the Special Issue Bioactive Lipids for Health Benefits)
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12 pages, 2707 KiB  
Article
Inhibition of Prostaglandin F2α Receptors Exaggerates HCl-Induced Lung Inflammation in Mice
by Toko Maehara and Ko Fujimori
Int. J. Mol. Sci. 2021, 22(23), 12843; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312843 - 27 Nov 2021
Cited by 6 | Viewed by 1900
Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe respiratory disorders that are caused by aspiration, sepsis, trauma, and pneumonia. A clinical feature of ALI/ARDS is the acute onset of severe hypoxemia, and the mortality rate, which is estimated at [...] Read more.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe respiratory disorders that are caused by aspiration, sepsis, trauma, and pneumonia. A clinical feature of ALI/ARDS is the acute onset of severe hypoxemia, and the mortality rate, which is estimated at 38–50%, remains high. Although prostaglandins (PGs) are detected in the bronchoalveolar lavage fluid of patients with ALI/ARDS, the role of PGF in ALI remains unclear. We aimed to clarify the role of PGF/PGF receptor (FP) signaling in acid-induced ALI using an FP receptor antagonist, AL8810. Intratracheal injection of hydrochloric acid (HCl) increased neutrophil migration into the lungs, leading to respiratory dysfunction. Pre-administration of AL8810 further increased these features. Moreover, pre-treatment with AL8810 enhanced the HCl-induced expression of pro-inflammatory cytokines and neutrophil migratory factors in the lungs. Administration of HCl decreased the gene expression of lung surfactant proteins, which was further reduced by co-administration of AL8810. Administration of AL8810 also increased lung edema and reduced mRNA expression of epithelial sodium channel in the lungs, indicating that AL8810 reduced fluid clearance. Furthermore, AL8810 also increased lipopolysaccharide-induced expression of adhesion molecules such as intracellular adhesion molecule-1 and E-selectin in human umbilical vein endothelial cells. These results indicate that inhibition of FP receptors by AL8810 exacerbated HCl-induced ALI. Full article
(This article belongs to the Special Issue Bioactive Lipids for Health Benefits)
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Review

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11 pages, 468 KiB  
Review
Pathogenic Role of the Sphingosine 1-Phosphate (S1P) Pathway in Common Gynecologic Disorders (GDs): A Possible Novel Therapeutic Target
by Alice Di Paolo, Arianna Vignini, Sonila Alia, Valentina Membrino, Giovanni Delli Carpini, Luca Giannella and Andrea Ciavattini
Int. J. Mol. Sci. 2022, 23(21), 13538; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232113538 - 04 Nov 2022
Cited by 5 | Viewed by 1661
Abstract
Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid, noteworthy for its involvement both in the modulation of various biological processes and in the development of many diseases. S1P signaling can be either pro or anti-inflammatory, and the sphingosine kinase (SphK)–S1P–S1P receptor (S1PR) axis is [...] Read more.
Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid, noteworthy for its involvement both in the modulation of various biological processes and in the development of many diseases. S1P signaling can be either pro or anti-inflammatory, and the sphingosine kinase (SphK)–S1P–S1P receptor (S1PR) axis is a factor in accelerating the growth of several cells, including endometriotic cells and fibrosis. Gynecologic disorders, including endometriosis, adenomyosis, and uterine fibroids are characterized by inflammation and fibrosis. S1P signaling and metabolism have been shown to be dysregulated in those disorders and they are likely implicated in their pathogenesis and pathophysiology. Enzymes responsible for inactivating S1P are the most affected by the dysregulation of S1P balanced levels, thus causing accumulation of sphingolipids within these cells and tissues. The present review highlights the past and latest evidence on the role played by the S1P pathways in common gynecologic disorders (GDs). Furthermore, it discusses potential future approaches in the regulation of this signaling pathway that could represent an innovative and promising therapeutical target, also for ovarian cancer treatment. Full article
(This article belongs to the Special Issue Bioactive Lipids for Health Benefits)
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