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Biomedicines
Special Issues
Sphingolipid Metabolism and Signaling in Health and Diseases: 2nd Edition
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Sphingolipid Metabolism and Signaling in Health and Diseases: 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 737

Special Issue Editors

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
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
Special Issues, Collections and Topics in MDPI journals
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 disor-ders; mitochondria
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. Giulia Lunghi
Dr. Elena Chiricozzi
Dr. Maria Fazzari
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

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Published Papers (1 paper)

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Research

19 pages, 3499 KiB  
Article
Acid Sphingomyelinase and Ceramide Signaling Pathway Mediates Nicotine-Induced NLRP3 Inflammasome Activation and Podocyte Injury
by Mohammad Atiqur Rahman, Sayantap Datta, Harini Lakkakula, Saisudha Koka and Krishna M. Boini
Biomedicines 2025, 13(2), 416; https://doi.org/10.3390/biomedicines13020416 - 9 Feb 2025
Viewed by 590
Abstract
Background: Recent studies have shown that Nlrp3 inflammasome activation is importantly involved in podocyte dysfunction induced by nicotine. The present study was designed to test whether acid sphingomyelinase (Asm) and ceramide signaling play a role in mediating nicotine-induced Nlrp3 inflammasome activation and subsequent [...] Read more.
Background: Recent studies have shown that Nlrp3 inflammasome activation is importantly involved in podocyte dysfunction induced by nicotine. The present study was designed to test whether acid sphingomyelinase (Asm) and ceramide signaling play a role in mediating nicotine-induced Nlrp3 inflammasome activation and subsequent podocyte damage. Methods and Results: Nicotine treatment significantly increased the Asm expression and ceramide production compared to control cells. However, prior treatment with amitriptyline, an Asm inhibitor significantly attenuated the nicotine-induced Asm expression and ceramide production. Confocal microscopic and biochemical analyses showed that nicotine treatment increased the colocalization of NLRP3 with Asc, Nlrp3 vs. caspase-1, IL-1? production, caspase-1 activity, and desmin expression in podocytes compared to control cells. Pretreatment with amitriptyline abolished the nicotine-induced colocalization of NLRP3 with Asc, Nlrp3 with caspase-1, IL-1? production, caspase-1 activity and desmin expression. Immunofluorescence analyses showed that nicotine treatment significantly decreased the podocin expression compared to control cells. However, prior treatment with amitriptyline attenuated the nicotine-induced podocin reduction. In addition, nicotine treatment significantly increased the cell permeability, O2 production, and apoptosis compared to control cells. However, prior treatment with amitriptyline significantly attenuated the nicotine-induced cell permeability, O2 production and apoptosis in podocytes. Conclusions: Asm is one of the important mediators of nicotine-induced inflammasome activation and podocyte injury. Asm may be a therapeutic target for the treatment or prevention of glomerulosclerosis associated with smoking. Full article
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Health and Diseases: 2nd Edition)
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Figure 1

Figure 1
<p>Asm inhibition attenuated nicotine-induced ceramide production. Representative immunofluorescence images (<b>A</b>) and quantification analysis (<b>B</b>) depicting ceramide expression in podocytes under different treatment conditions, including nicotine stimulation and/or amitriptyline, an Asm inhibitor. Image quantification was performed using ImageJ software. N = 20. * Indicates a significant difference compared to the control group, while # denotes a significant difference from the nicotine-treated group.</p> Full article ">Figure 2
<p>Asm inhibition attenuated nicotine-induced Asm expression and activity. Analysis of acid sphingomyelinase (Asm) activity (<b>A</b>) and expression (<b>B</b>) in podocytes treated with nicotine and/or amitriptyline, an Asm inhibitor. Immunofluorescence images were quantified using ImageJ software. N = 20 for immunofluorescence analysis. * Represents a significant difference from the control group, while # indicates a significant difference from the nicotine-treated group.</p> Full article ">Figure 3
<p>Inhibition of Asm attenuated nicotine-induced inflammasomes formation in podocytes. Confocal images representing the colocalization of Nlrp3 (green) with Caspase-1 (red) (<b>A</b>) and Nlrp3 (green) with Asc (red) (<b>C</b>) in podocytes (original magnification ×100). Summarized data showing the fold change of the Pearson coefficient correlation (PCC) for the colocalization of Nlrp3 with caspase-1 (<b>B</b>) and Nlrp3 with Asc (<b>D</b>). Ctrl: control, Veh: vehicle, Ami: amitriptyline. Images were quantified using Image Pro Plus software. N = 18–20. * Significant difference from the control, # Significant difference from the nicotine-treated group.</p> Full article ">Figure 4
<p>Inhibition of Asm attenuated nicotine-induced inflammasomes activation in podocytes. Data are presented as arithmetic means ± SEM (n = 6 per group) for IL-1β production (<b>A</b>) and caspase-1 activity (<b>B</b>) in podocytes exposed to nicotine, with or without amitriptyline, an Asm inhibitor. * Significant difference from the control, # Significant difference from the nicotine-treated group.</p> Full article ">Figure 5
<p>Inhibition of Asm attenuated nicotine-induced podocytes damage. Confocal images represent the expressions of Podocin (<b>A</b>) and summarized quantification of Podocin (<b>B</b>). Western Blot data show the expression of Podocin (<b>C</b>) and summarized quantification of Podocin (<b>D</b>). N = 15–20 each group for immunofluorescence expression. Ctrl: control, Veh: vehicle, Ami: amitriptyline. Image analysis was performed using ImageJ software. * Indicates a significant difference from the control group, while # denotes a significant difference from the nicotine-treated group.</p> Full article ">Figure 6
<p>Inhibition of Asm attenuated nicotine-induced podocytes damage. Confocal images represent the expressions of desmin (<b>A</b>) and summarized quantification of desmin (<b>B</b>). Western blot data show the expression of desmin (<b>C</b>) and summarized quantification of desmin (<b>D</b>). N = 15–20 each group for immunofluorescence expression. Ctrl: control, Veh: vehicle, Ami: amitriptyline. Images were quantified using Image J software. * Significant difference from the control; # significant difference from the nicotine-treated group.</p> Full article ">Figure 7
<p>Suppression of Asm effectively reduced nicotine-induced increases in podocyte permeability. Data are presented as arithmetic means ± SEM (n = 9 per group) for podocyte permeability in podocytes with or without nicotine stimulation and/or amitriptyline, an Asm inhibitor. * Indicates a significant difference from the control group, while # denotes a significant difference from the nicotine-treated group.</p> Full article ">Figure 8
<p>O<sub>2</sub>.<sup>−</sup> Production in podocytes with or without nicotine and/or amitriptyline treatment. Values are arithmetic means ± SE (n = 6 each group) of O<sub>2</sub>.<sup>−</sup> production in podocytes with or without nicotine and/or amitriptyline treatment. Ctrl: control, * significant difference (<span class="html-italic">p</span> &lt; 0.05) compared to the control group; # significant difference from the nicotine-treated group.</p> Full article ">Figure 9
<p>Inhibition of Asm protects against nicotine-induced apoptosis in podocytes. Flow cytometry analysis (<b>A</b>) and corresponding quantification (<b>B</b>) were performed to investigate the role of Asm in nicotine-mediated podocyte apoptosis. Data were analyzed using FlowJo v10.10.0 software, with apoptotic cells (%) calculated as the sum of early apoptotic, late apoptotic, and necrotic populations. Results are presented as fold change relative to the control group. * <span class="html-italic">p</span> &lt; 0.05 vs. control group, <span class="html-italic">p</span> &lt; 0.05 vs. nicotine-treated group; <sup>#</sup> significant difference from the nicotine-treated group. Q1: necrotic cells, Q2: late apoptotic cells, Q3: early apoptotic cells, Q4: live cells, Ctrl: control podocytes, Nico: nicotine (8 µM)-treated podocytes.</p> Full article ">
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