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Biomedicines
Special Issues
Sphingolipid Metabolism and Signaling in Health and Diseases
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Sphingolipid Metabolism and Signaling in Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 7396

Special Issue Editors

Dr. Maria Fazzari

E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Interests: gangliosides; GM1 ganglioside; neurodegenerative and neurodevelopmental disorders; mitochondria
Dr. Elena Chiricozzi

E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Interests: glycosphingolipids; gangliosides; GM1; GM1 oligosaccharide; plasma membrane signaling; neuronal disease; Parkinson’s disease
Dr. Giulia Lunghi

E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy
Interests: sphingolipids; neurodegenerative disorders; GM1 ganglioside; lysosomes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Sphingolipids are a class of lipids highly expressed in eukaryotic cells, where they represent key components of membranes. In addition to their structural role, they act as bioactive molecules capable of modulating intracellular signaling and, accordingly, several cell functions, including cell proliferation, differentiation, migration and apoptosis. Consequently, alterations in sphingolipid metabolism and signaling have been associated with several pathological conditions, spanning from neurodegeneration to cancer and diabetes. However, a complete comprehension of the molecular mechanism by which sphingolipids regulate cell homeostasis is still lacking. Providing new information about sphingolipid signaling and metabolism is pivotal for addressing their role both in health and in diseases.

In this Special Issue “Sphingolipid Metabolism and Signaling in Health and Disease”, we aim to collect original research and review articles regarding the role of sphingolipids in modulating cellular functions in different physiopathological conditions.

Dr. Maria Fazzari
Dr. Elena Chiricozzi
Dr. Giulia Lunghi
Guest Editors

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. Biomedicines 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 2600 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

  • sphingolipids
  • glycosphingolipids
  • gangliosides
  • sphingosine-1-phosphate
  • cell homeostasis
  • neurodegeneration
  • neurodevelopment
  • inflammation
  • diabetes
  • cystic fibrosis
  • cancer

Published Papers (5 papers)

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Research

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14 pages, 1789 KiB  
Article
GM1 Oligosaccharide Efficacy in Parkinson’s Disease: Protection against MPTP
by Maria Fazzari, Giulia Lunghi, Alexandre Henriques, Noëlle Callizot, Maria Grazia Ciampa, Laura Mauri, Simona Prioni, Emma Veronica Carsana, Nicoletta Loberto, Massimo Aureli, Luigi Mari, Sandro Sonnino, Elena Chiricozzi and Erika Di Biase
Biomedicines 2023, 11(5), 1305; https://doi.org/10.3390/biomedicines11051305 - 28 Apr 2023
Cited by 2 | Viewed by 1225
Abstract
Past evidence has shown that the exogenous administration of GM1 ganglioside slowed neuronal death in preclinical models of Parkinson’s disease, a neurodegenerative disorder characterized by the progressive loss of dopamine-producing neurons: however, the physical and chemical properties of GM1 (i.e., amphiphilicity) limited its [...] Read more.
Past evidence has shown that the exogenous administration of GM1 ganglioside slowed neuronal death in preclinical models of Parkinson’s disease, a neurodegenerative disorder characterized by the progressive loss of dopamine-producing neurons: however, the physical and chemical properties of GM1 (i.e., amphiphilicity) limited its clinical application, as the crossing of the blood–brain barrier is denied. Recently, we demonstrated that the GM1 oligosaccharide head group (GM1-OS) is the GM1 bioactive portion that, interacting with the TrkA-NGF complex at the membrane surface, promotes the activation of a multivariate network of intracellular events regulating neuronal differentiation, protection, and reparation. Here, we evaluated the GM1-OS neuroprotective potential against the Parkinson’s disease-linked neurotoxin MPTP, which destroys dopaminergic neurons by affecting mitochondrial bioenergetics and causing ROS overproduction. In dopaminergic and glutamatergic primary cultures, GM1-OS administration significantly increased neuronal survival, preserved neurite network, and reduced mitochondrial ROS production enhancing the mTOR/Akt/GSK3β pathway. These data highlight the neuroprotective efficacy of GM1-OS in parkinsonian models through the implementation of mitochondrial function and reduction in oxidative stress. Full article
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Health and Diseases)
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19 pages, 1830 KiB  
Article
Distinct Changes in Placental Ceramide Metabolism Characterize Type 1 and 2 Diabetic Pregnancies with Fetal Macrosomia or Preeclampsia
by Miira M. Klemetti, Sruthi Alahari, Martin Post and Isabella Caniggia
Biomedicines 2023, 11(3), 932; https://doi.org/10.3390/biomedicines11030932 - 17 Mar 2023
Cited by 1 | Viewed by 1373
Abstract
Disturbances of lipid metabolism are typical in diabetes. Our objective was to characterize and compare placental sphingolipid metabolism in type 1 (T1D) and 2 (T2D) diabetic pregnancies and in non-diabetic controls. Placental samples from T1D, T2D, and control pregnancies were processed for sphingolipid [...] Read more.
Disturbances of lipid metabolism are typical in diabetes. Our objective was to characterize and compare placental sphingolipid metabolism in type 1 (T1D) and 2 (T2D) diabetic pregnancies and in non-diabetic controls. Placental samples from T1D, T2D, and control pregnancies were processed for sphingolipid analysis using tandem mass spectrometry. Western blotting, enzyme activity, and immunofluorescence analyses were used to study sphingolipid regulatory enzymes. Placental ceramide levels were lower in T1D and T2D compared to controls, which was associated with an upregulation of the ceramide degrading enzyme acid ceramidase (ASAH1). Increased placental ceramide content was found in T1D complicated by preeclampsia. Similarly, elevated ceramides were observed in T1D and T2D pregnancies with poor glycemic control. The protein levels and activity of sphingosine kinases (SPHK) that produce sphingoid-1-phosphates (S1P) were highest in T2D. Furthermore, SPHK levels were upregulated in T1D and T2D pregnancies with fetal macrosomia. In vitro experiments using trophoblastic JEG3 cells demonstrated increased SPHK expression and activity following glucose and insulin treatments. Specific changes in the placental sphingolipidome characterize T1D and T2D placentae depending on the type of diabetes and feto-maternal complications. Increased exposure to insulin and glucose is a plausible contributor to the upregulation of the SPHK-S1P-axis in diabetic placentae. Full article
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Health and Diseases)
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11 pages, 2796 KiB  
Article
Age-Related Decline in Gangliosides GM1 and GD1a in Non-CNS Tissues of Normal Mice: Implications for Peripheral Symptoms of Parkinson’s Disease
by Suman Chowdhury, Gusheng Wu, Zi-Hua Lu, Ranjeet Kumar and Robert Ledeen
Biomedicines 2023, 11(1), 209; https://doi.org/10.3390/biomedicines11010209 - 14 Jan 2023
Cited by 5 | Viewed by 1488
Abstract
The purpose of this study was to determine whether the age-related decline in a-series gangliosides (especially GM1), shown to be a factor in the brain-related etiology of Parkinson’s disease (PD), also pertains to the peripheral nervous system (PNS) and aspects of PD unrelated [...] Read more.
The purpose of this study was to determine whether the age-related decline in a-series gangliosides (especially GM1), shown to be a factor in the brain-related etiology of Parkinson’s disease (PD), also pertains to the peripheral nervous system (PNS) and aspects of PD unrelated to the central nervous system (CNS). Following Svennerholm’s demonstration of the age-dependent decline in a-series gangliosides (both GM1 and GD1a) in the human brain, we previously demonstrated a similar decline in the normal mouse brain. The present study seeks to determine whether a similar a-series decline occurs in the periphery of normal mice as a possible prelude to the non-CNS symptoms of PD. We used mice of increasing age to measure a-series gangliosides in three peripheral tissues closely associated with PD pathology. Employing high-performance thin-layer chromatography (HPTLC), we found a substantial decrease in both GM1 and GD1a in all three tissues from 191 days of age. Motor and cognitive dysfunction were also shown to worsen, as expected, in synchrony with the decrease in GM1. Based on the previously demonstrated parallel between mice and humans concerning age-related a-series ganglioside decline in the brain, we propose the present findings to suggest a similar a-series decline in human peripheral tissues as the primary contributor to non-CNS pathologies of PD. An onset of sporadic PD would thus be seen as occurring simultaneously throughout the brain and body, albeit at varying rates, in association with the decline in a-series gangliosides. This would obviate the need to postulate the transfer of aggregated α-synuclein between brain and body or to debate brain vs. body as the origin of PD. Full article
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Health and Diseases)
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11 pages, 1075 KiB  
Article
Interorgan Metabolism of Ganglioside Is Altered in Type 2 Diabetes
by Irma Magaly Rivas Serna, Michelle Beveridge, Michaelann Wilke, Edmond A. Ryan, Michael Thomas Clandinin and Vera Christine Mazurak
Biomedicines 2022, 10(12), 3141; https://doi.org/10.3390/biomedicines10123141 - 06 Dec 2022
Cited by 1 | Viewed by 1347
Abstract
GM3 is implicated in cell signaling, inflammation and insulin resistance. The intestinal mucosa metabolizes ganglioside and provides gangliosides for uptake by peripheral tissues. Gangliosides downregulate acute and chronic inflammatory signals. It is likely that transport of intestinal derived gangliosides to other tissues impact [...] Read more.
GM3 is implicated in cell signaling, inflammation and insulin resistance. The intestinal mucosa metabolizes ganglioside and provides gangliosides for uptake by peripheral tissues. Gangliosides downregulate acute and chronic inflammatory signals. It is likely that transport of intestinal derived gangliosides to other tissues impact the same signals characteristic of inflammatory change in other chronic conditions such as Type 2 Diabetes (T2DM). The postprandial ceramide composition of GM3 and other gangliosides in plasma and chylomicrons has not been examined in T2DM. The present study assessed if diet or T2DM alters ganglioside components in plasma and chylomicrons secreted from the intestinal mucosa after a meal. GD1, GD3, and GM3 content of chylomicrons and plasma was determined by LC/triple quad MS in non-diabetic (control) and T2DM individuals in the fasting and postprandial state after 2 days of consuming a low or high fat diet in a randomized blinded crossover design. Diet fat level did not alter baseline plasma or chylomicron ganglioside levels. Four hours after the test meal, plasma monounsaturated GD3 was 75% higher, plasma saturated GD3 was 140% higher and plasma polyunsaturated GM3 30% lower in diabetic subjects compared to control subjects. At 4 h, chylomicron GD1 was 50% lower in T2DM compared to controls. The proportion of d34:1 in GD3 was more abundant and d36:1 in GD1 less abundant in T2DM compared to control subjects at 4 h. The present study indicates that T2DM alters ceramide composition of ganglioside available for uptake by peripheral tissues. Full article
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Health and Diseases)
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Review

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16 pages, 1876 KiB  
Review
The Role of Sphingolipids in Regulating Vascular Permeability in Idiopathic Pulmonary Fibrosis
by Girish Jayant, Stephen Kuperberg, Kaumudi Somnay and Raj Wadgaonkar
Biomedicines 2023, 11(6), 1728; https://doi.org/10.3390/biomedicines11061728 - 16 Jun 2023
Cited by 1 | Viewed by 1348
Abstract
Idiopathic pulmonary fibrosis (IPF) is a disease that causes scarring and fibrotic transformation of the lung parenchyma, resulting in the progressive loss of respiratory function and, often, death. Current treatments that target profibrotic factors can slow the rate of progression but are unable [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a disease that causes scarring and fibrotic transformation of the lung parenchyma, resulting in the progressive loss of respiratory function and, often, death. Current treatments that target profibrotic factors can slow the rate of progression but are unable to ultimately stop it. In the past decade, many studies have shown that increased vascular permeability may be both a predictive and perpetuating factor in fibrogenesis. Consequently, there is a search for therapeutic targets to try and modulate vascular permeability in fibrotic lungs. One such class of targets that show great promise is sphingolipids. Sphingolipids are common in cell membranes and are increasingly recognized as critical to many cell signaling pathways, including those that affect the integrity of the vascular endothelial barrier. In this focused review we look at sphingolipids, particularly the sphingosine-1-phosphate (S1P) axis and its effects on vascular permeability, and how those effects may affect the pathogenesis of IPF. We further examine existing S1P modulators and their potential efficacy as therapeutics for IPF. Full article
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Health and Diseases)
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