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Cells
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Lipid Signalling and Metabolism in Inflammation-Associated Pathologies
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Lipid Signalling and Metabolism in Inflammation-Associated Pathologies

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 16433

Special Issue Editor

Prof. Dr. Klaus Scholich

E-Mail Website1 Website2
Guest Editor
1. Institute for Clinical Pharmacology, Hospital of the Goethe University Frankfurt, Germany;
2. Pain Pharmacology, Fraunhofer Institute IME-TMP, Frankfurt, Germany
Interests: lipid signalling; inflammation; pain; neuropathies; resolution of inflammation; macrophages; diabetes

Special Issue Information

Dear Colleagues,

Lipids are essential parts of cellular structures including plasma membranes and all intracellular organelles such as the ER, the Golgi apparatus, lysosomes, mitochondria, etc. In addition, they play key roles in many intra- and extracellular signalling events which take place in homeostasis and under most pathological conditions. Especially, their crucial roles in diseases with an inflammatory component (e.g., cancer, autoimmune diseases, neuropathies or atherosclerosis) have raised increasing interest in lipid-generating enzymes and lipid receptors as potential drug targets. This is reflected by the fact that some of the drugs that are most used globally target lipid synthesis or lipid receptors.

In this Special Issue of Cells, we invite your contributions, either in the form of original research articles or reviews, on all aspects related to lipid synthesis and signalling as well as their functions in inflammation-associated pathologies in human diseases or their animal models. Articles giving new structural, mechanistic or functional insights from the cellular or in vivo perspective are welcome.

Relevant topics include, but are not limited to:

  • Genetic and epigenetic regulation of proteins involved in lipid synthesis or their signalling pathways;
  • Cellular and molecular mechanisms of lipid signalling;
  • Contribution of lipid mediators to innate and adaptive immunity;
  • Lipid signalling and metabolism in tumour models;
  • Regulation of vascular functions and atherosclerosis by lipids;
  • Contribution of lipids to inflammatory and neuropathic pain;
  • Regulation of adipocyte functions;
  • Role of lipid signalling in diabetes;
  • “Multi-omics” analysis of lipid contributions to diseases;
  • Translational aspects of lipid signalling and metabolism.

We look forward to your manuscript submissions.

Prof. Dr. Klaus Scholich
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. Cells is an international peer-reviewed open access semimonthly 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
  • signalling
  • metabolism
  • receptors
  • ion channels
  • inflammation
  • cancer
  • pain
  • diabetes
  • atherosclerosis
  • immune cells
  • adipocytes

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Published Papers (4 papers)

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Research

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20 pages, 4172 KiB  
Article
AGMO Inhibitor Reduces 3T3-L1 Adipogenesis
by Caroline Fischer, Annett Wilken-Schmitz, Victor Hernandez-Olmos, Ewgenij Proschak, Holger Stark, Ingrid Fleming, Andreas Weigert, Manuela Thurn, Martine Hofmann, Ernst R. Werner, Gerd Geisslinger, Ellen Niederberger, Katrin Watschinger and Irmgard Tegeder
Cells 2021, 10(5), 1081; https://doi.org/10.3390/cells10051081 - 1 May 2021
Cited by 6 | Viewed by 3338
Abstract
Alkylglycerol monooxygenase (AGMO) is a tetrahydrobiopterin (BH4)-dependent enzyme with major expression in the liver and white adipose tissue that cleaves alkyl ether glycerolipids. The present study describes the disclosure and biological characterization of a candidate compound (Cp6), which inhibits AGMO with an IC50 [...] Read more.
Alkylglycerol monooxygenase (AGMO) is a tetrahydrobiopterin (BH4)-dependent enzyme with major expression in the liver and white adipose tissue that cleaves alkyl ether glycerolipids. The present study describes the disclosure and biological characterization of a candidate compound (Cp6), which inhibits AGMO with an IC50 of 30–100 µM and 5–20-fold preference of AGMO relative to other BH4-dependent enzymes, i.e., phenylalanine-hydroxylase and nitric oxide synthase. The viability and metabolic activity of mouse 3T3-L1 fibroblasts, HepG2 human hepatocytes and mouse RAW264.7 macrophages were not affected up to 10-fold of the IC50. However, Cp6 reversibly inhibited the differentiation of 3T3-L1 cells towards adipocytes, in which AGMO expression was upregulated upon differentiation. Cp6 reduced the accumulation of lipid droplets in adipocytes upon differentiation and in HepG2 cells exposed to free fatty acids. Cp6 also inhibited IL-4-driven differentiation of RAW264.7 macrophages towards M2-like macrophages, which serve as adipocyte progenitors in adipose tissue. Collectively, the data suggest that pharmacologic AGMO inhibition may affect lipid storage. Full article
(This article belongs to the Special Issue Lipid Signalling and Metabolism in Inflammation-Associated Pathologies)
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17 pages, 1985 KiB  
Article
Exercise-Induced Changes in Bioactive Lipids Might Serve as Potential Predictors of Post-Exercise Hypotension. A Pilot Study in Healthy Volunteers
by Miriam C. Wolters, Julia Schmetzer, Christine V. Möser, Lisa Hahnefeld, Carlo Angioni, Dominique Thomas, Nerea Ferreirós, Gerd Geisslinger and Ellen Niederberger
Cells 2020, 9(9), 2111; https://doi.org/10.3390/cells9092111 - 16 Sep 2020
Cited by 1 | Viewed by 2487
Abstract
Post-exercise hypotension (PEH) is the phenomenon of lowered blood pressure after a single bout of exercise. Only a fraction of people develops PEH but its occurrence correlates well with long-term effects of sports on blood pressure. Therefore, PEH has been suggested as a [...] Read more.
Post-exercise hypotension (PEH) is the phenomenon of lowered blood pressure after a single bout of exercise. Only a fraction of people develops PEH but its occurrence correlates well with long-term effects of sports on blood pressure. Therefore, PEH has been suggested as a suitable predictor for the effectivity of exercise as therapy in hypertension. Local vascular bioactive lipids might play a potential role in this context. We performed a cross-over clinical pilot study with 18 healthy volunteers to investigate the occurrence of PEH after a single short-term endurance exercise. Furthermore, we investigated the plasma lipid profile with focus on arachidonic acid (AA)-derived metabolites as potential biomarkers of PEH. A single bout of ergometer cycling induced a significant PEH in healthy volunteers with the expected high inter-individual variability. Targeted lipid spectrum analysis revealed significant upregulation of several lipids in the direct post-exercise phase. Among these changes, only 15- hydroxyeicosatetranoic acid (HETE) correlated significantly with the extent of PEH but in an AA-independent manner, suggesting that 15-HETE might act as specific PEH-marker. Our data indicate that specific lipid modulation might facilitate the identification of patients who will benefit from exercise activity in hypertension therapy. However, larger trials including hypertonic patients are necessary to verify the clinical value of this hypothesis. Full article
(This article belongs to the Special Issue Lipid Signalling and Metabolism in Inflammation-Associated Pathologies)
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18 pages, 2268 KiB  
Article
The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain
by Tabea Osthues, Béla Zimmer, Vittoria Rimola, Kevin Klann, Karin Schilling, Praveen Mathoor, Carlo Angioni, Andreas Weigert, Gerd Geisslinger, Christian Münch, Klaus Scholich and Marco Sisignano
Cells 2020, 9(7), 1740; https://doi.org/10.3390/cells9071740 - 21 Jul 2020
Cited by 17 | Viewed by 5566
Abstract
Nerve injury-induced neuropathic pain is difficult to treat and mechanistically characterized by strong neuroimmune interactions, involving signaling lipids that act via specific G-protein coupled receptors. Here, we investigated the role of the signaling lipid receptor G2A (GPR132) in nerve injury-induced neuropathic pain using [...] Read more.
Nerve injury-induced neuropathic pain is difficult to treat and mechanistically characterized by strong neuroimmune interactions, involving signaling lipids that act via specific G-protein coupled receptors. Here, we investigated the role of the signaling lipid receptor G2A (GPR132) in nerve injury-induced neuropathic pain using the robust spared nerve injury (SNI) mouse model. We found that the concentrations of the G2A agonist 9-HODE (9-Hydroxyoctadecadienoic acid) are strongly increased at the site of nerve injury during neuropathic pain. Moreover, G2A-deficient mice show a strong reduction of mechanical hypersensitivity after nerve injury. This phenotype is accompanied by a massive reduction of invading macrophages and neutrophils in G2A-deficient mice and a strongly reduced release of the proalgesic mediators TNFα, IL-6 and VEGF at the site of injury. Using a global proteome analysis to identify the underlying signaling pathways, we found that G2A activation in macrophages initiates MyD88-PI3K-AKT signaling and transient MMP9 release to trigger cytoskeleton remodeling and migration. We conclude that G2A-deficiency reduces inflammatory responses by decreasing the number of immune cells and the release of proinflammatory cytokines and growth factors at the site of nerve injury. Inhibiting the G2A receptor after nerve injury may reduce immune cell-mediated peripheral sensitization and may thus ameliorate neuropathic pain. Full article
(This article belongs to the Special Issue Lipid Signalling and Metabolism in Inflammation-Associated Pathologies)
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Review

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13 pages, 1419 KiB  
Review
The Anti-Infectious Role of Sphingosine in Microbial Diseases
by Yuqing Wu, Yongjie Liu, Erich Gulbins and Heike Grassmé
Cells 2021, 10(5), 1105; https://doi.org/10.3390/cells10051105 - 4 May 2021
Cited by 24 | Viewed by 4234
Abstract
Sphingolipids are important structural membrane components and, together with cholesterol, are often organized in lipid rafts, where they act as signaling molecules in many cellular functions. They play crucial roles in regulating pathobiological processes, such as cancer, inflammation, and infectious diseases. The bioactive [...] Read more.
Sphingolipids are important structural membrane components and, together with cholesterol, are often organized in lipid rafts, where they act as signaling molecules in many cellular functions. They play crucial roles in regulating pathobiological processes, such as cancer, inflammation, and infectious diseases. The bioactive metabolites ceramide, sphingosine-1-phosphate, and sphingosine have been shown to be involved in the pathogenesis of several microbes. In contrast to ceramide, which often promotes bacterial and viral infections (for instance, by mediating adhesion and internalization), sphingosine, which is released from ceramide by the activity of ceramidases, kills many bacterial, viral, and fungal pathogens. In particular, sphingosine is an important natural component of the defense against bacterial pathogens in the respiratory tract. Pathologically reduced sphingosine levels in cystic fibrosis airway epithelial cells are normalized by inhalation of sphingosine, and coating plastic implants with sphingosine prevents bacterial infections. Pretreatment of cells with exogenous sphingosine also prevents the viral spike protein of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) from interacting with host cell receptors and inhibits the propagation of herpes simplex virus type 1 (HSV-1) in macrophages. Recent examinations reveal that the bactericidal effect of sphingosine might be due to bacterial membrane permeabilization and the subsequent death of the bacteria. Full article
(This article belongs to the Special Issue Lipid Signalling and Metabolism in Inflammation-Associated Pathologies)
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