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Metabolites
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Prostaglandin Metabolites
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Prostaglandin Metabolites

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Lipid Metabolism".

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 7728

Special Issue Editor

Dr. Helena Idborg

E-Mail Website
Guest Editor
Rheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden
Interests: metabolomics; screening of biomarkers; drug metabolites; lipidomics; proteomics; mass spectrometry; liquid chromatography; biostatistics; multivariate data analysis

Special Issue Information

Dear colleagues,

Prostaglandins are bioactive signaling lipids involved in different biological activities and diseases, and the discovery of these compounds was awarded the Nobel Prize for Physiology or Medicine in 1982, highlighting their importance. These compounds are unstable, and many downstream metabolites have been shown to have additional functions and be involved in feedback mechanisms. Important research regarding prostaglandin metabolites has been carried out in various fields, but consensus has not always been reached, and several questions remain to be answered. What known and novel metabolites can be detected in a certain tissue and what type of functions do they have under a certain condition, in a certain cell type, and in a certain species? Do specific metabolites have different functions in different diseases, and what is the common profile of metabolites? Do the metabolites originate from local production or systemic biosynthesis? Can prostaglandin metabolites be used as biomarkers for disease progression and response to treatment? By combining scientific work performed within different disciplines with focus on prostaglandin metabolites, knowledge in metabolite functions will be enhanced and facilitated by this Special Issue.

This Special Issue welcomes the submission of papers describing biosynthesis, characterization, and function of prostaglandin metabolites. Clinical applications and biomarker studies performed on these metabolites are of great interest, as well as methodological improvement for detection of prostaglandin metabolites. Knowledge in the interaction between different eicosanoids and their functions in comparable models are relevant and studies on other metabolites in the arachidonic acid cascade might also be taken into consideration for publication in this issue.

Dr. Helena Idborg
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lipid mediators
  • bioactive lipids
  • lipidomics
  • metabolic profiling
  • arachidonic acid cascade
  • eicosanoids
  • prostanoids
  • unsaturated fatty acids
  • inflammation
  • resolution
  • biomarkers
  • functional studies
  • drug targets
  • inhibitors
  • biosynthesis
  • pathology
  • phenotyping

Published Papers (3 papers)

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Research

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16 pages, 2925 KiB  
Article
PPARβ/δ Augments IL-1β-Induced COX-2 Expression and PGE2 Biosynthesis in Human Mesangial Cells via the Activation of SIRT1
by Yaqing Li, Rong Cao, Tingting Gu, Cong Cao, Tingyue Chen, Youfei Guan and Xiaoyan Zhang
Metabolites 2022, 12(7), 595; https://doi.org/10.3390/metabo12070595 - 27 Jun 2022
Cited by 5 | Viewed by 1673
Abstract
Peroxisome proliferator-activated receptor β/δ (PPARβ/δ), a ligand-activated nuclear receptor, regulates lipid and glucose metabolism and inflammation. PPARβ/δ can exert an anti-inflammatory effect by suppressing proinflammatory cytokine production. Cyclooxygenase-2 (COX-2)-triggered inflammation plays a crucial role in the development of many inflammatory diseases, including glomerulonephritis. [...] Read more.
Peroxisome proliferator-activated receptor β/δ (PPARβ/δ), a ligand-activated nuclear receptor, regulates lipid and glucose metabolism and inflammation. PPARβ/δ can exert an anti-inflammatory effect by suppressing proinflammatory cytokine production. Cyclooxygenase-2 (COX-2)-triggered inflammation plays a crucial role in the development of many inflammatory diseases, including glomerulonephritis. However, the effect of PPARβ/δ on the expression of COX-2 in the kidney has not been fully elucidated. The present study showed that PPARβ/δ was functionally expressed in human mesangial cells (hMCs), where its expression was increased by interleukin-1β (IL-1β) treatment concomitant with enhanced COX-2 expression and prostaglandin E2 (PGE2) biosynthesis. The treatment of hMCs with GW0742, a selective agonist of PPARβ/δ, or the overexpression of PPARβ/δ via an adenovirus-mediated approach significantly increased COX-2 expression and PGE2 production. PPARβ/δ could further augment the IL-1β-induced COX-2 expression and PGE2 production in hMCs. Moreover, both PPARβ/δ activation and overexpression markedly increased sirtuin 1 (SIRT1) expression. The inhibition or knockdown of SIRT1 significantly attenuated the effects of PPARβ/δ on the IL-1β-induced expression of COX-2 and PGE2 biosynthesis. Taken together, PPARβ/δ could augment the IL-1β-induced COX-2 expression and PGE2 production in hMCs via the SIRT1 pathway. Given the critical role of COX-2 in glomerulonephritis, PPARβ/δ may represent a novel target for the treatment of renal inflammatory diseases. Full article
(This article belongs to the Special Issue Prostaglandin Metabolites)
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21 pages, 2733 KiB  
Article
Knock-In Mice Expressing a 15-Lipoxygenating Alox5 Mutant Respond Differently to Experimental Inflammation Than Reported Alox5−/− Mice
by Eugenia Marbach-Breitrück, Nadine Rohwer, Carmen Infante-Duarte, Silvina Romero-Suarez, Dominika Labuz, Halina Machelska, Laura Kutzner, Nils Helge Schebb, Michael Rothe, Pallu Reddanna, Karsten H. Weylandt, Lothar H. Wieler, Dagmar Heydeck and Hartmut Kuhn
Metabolites 2021, 11(10), 698; https://doi.org/10.3390/metabo11100698 - 12 Oct 2021
Cited by 9 | Viewed by 2703
Abstract
Arachidonic acid 5-lipoxygenase (ALOX5) is the key enzyme in the biosynthesis of pro-inflammatory leukotrienes. We recently created knock-in mice (Alox5-KI) which express an arachidonic acid 15-lipoxygenating Alox5 mutant instead of the 5-lipoxygenating wildtype enzyme. These mice were leukotriene deficient but exhibited [...] Read more.
Arachidonic acid 5-lipoxygenase (ALOX5) is the key enzyme in the biosynthesis of pro-inflammatory leukotrienes. We recently created knock-in mice (Alox5-KI) which express an arachidonic acid 15-lipoxygenating Alox5 mutant instead of the 5-lipoxygenating wildtype enzyme. These mice were leukotriene deficient but exhibited an elevated linoleic acid oxygenase activity. Here we characterized the polyenoic fatty acid metabolism of these mice in more detail and tested the animals in three different experimental inflammation models. In experimental autoimmune encephalomyelitis (EAE), Alox5-KI mice displayed an earlier disease onset and a significantly higher cumulative incidence rate than wildtype controls but the clinical score kinetics were not significantly different. In dextran sodium sulfate-induced colitis (DSS) and in the chronic constriction nerve injury model (CCI), Alox5-KI mice performed like wildtype controls with similar genetic background. These results were somewhat surprising since in previous loss-of-function studies targeting leukotriene biosynthesis (Alox5−/− mice, inhibitor studies), more severe inflammatory symptoms were observed in the EAE model but the degree of inflammation in DSS colitis was attenuated. Taken together, our data indicate that these mutant Alox5-KI mice respond differently in two models of experimental inflammation than Alox5−/− animals tested previously in similar experimental setups. Full article
(This article belongs to the Special Issue Prostaglandin Metabolites)
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Review

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25 pages, 1835 KiB  
Review
Prostanoid Metabolites as Biomarkers in Human Disease
by Helena Idborg and Sven-Christian Pawelzik
Metabolites 2022, 12(8), 721; https://doi.org/10.3390/metabo12080721 - 04 Aug 2022
Cited by 13 | Viewed by 2691
Abstract
Prostaglandins (PGD2, PGE2, PGF2α), prostacyclin (PGI2), and thromboxane A2 (TXA2) together form the prostanoid family of lipid mediators. As autacoids, these five primary prostanoids propagate intercellular signals and are involved in [...] Read more.
Prostaglandins (PGD2, PGE2, PGF2α), prostacyclin (PGI2), and thromboxane A2 (TXA2) together form the prostanoid family of lipid mediators. As autacoids, these five primary prostanoids propagate intercellular signals and are involved in many physiological processes. Furthermore, alterations in their biosynthesis accompany a wide range of pathological conditions, which leads to substantially increased local levels during disease. Primary prostanoids are chemically instable and rapidly metabolized. Their metabolites are more stable, integrate the local production on a systemic level, and their analysis in various biological matrices yields valuable information under different pathological settings. Therefore, prostanoid metabolites may be used as diagnostic, predictive, or prognostic biomarkers in human disease. Although their potential as biomarkers is great and extensive research has identified major prostanoid metabolites that serve as target analytes in different biofluids, the number of studies that correlate prostanoid metabolite levels to disease outcome is still limited. We review the metabolism of primary prostanoids in humans, summarize the levels of prostanoid metabolites in healthy subjects, and highlight existing biomarker studies. Since analysis of prostanoid metabolites is challenging because of ongoing metabolism and limited half-lives, an emphasis of this review lies on the reliable measurement and interpretation of obtained levels. Full article
(This article belongs to the Special Issue Prostaglandin Metabolites)
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