Biomembranes and Cell Signaling in Health and Disease

A special issue of Membranes (ISSN 2077-0375). This special issue belongs to the section "Biological Membrane Functions".

Deadline for manuscript submissions: closed (20 December 2021) | Viewed by 7619

Special Issue Editors


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Guest Editor
Laboratory of Biochemistry, Department of Chemistry, University of Ioannina, 45110 Ioannina, Greece
Interests: lipid biochemistry; lipid analysis; biological membranes; extracellular vesicles; lung surfactant; phospholipase A2

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Guest Editor
Faculty of Medicine, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
Interests: modelling of axonal growth and filopodia dynamics; neuronal/axonal growth; lipid signalling; pharmacological targeting

Special Issue Information

Dear Colleagues,

Biological membranes are dynamic and complex structures of phospholipids and proteins, including lower amounts of neutral lipids and carbohydrates. Their role is not restricted to the preservation of the integrity of cells and cell organelles; they also have an active involvement in important biological functions through alterations of molecular composition and physicochemical properties in the entire membrane or in specific patches that facilitate the activation of signaling processes or the maintenance of homeostasis.

The aim of this Special Issue is to present the state of the art in the contribution of biological membranes in cellular homeostasis, in the pathophysiology of serious disorders such as inflammation, cancer, and age-related diseases, and in diagnostic or therapeutic schemes and strategies.

In this frame, the response and adaptation of cells to physical and chemical environmental conditions, changes in the cytoskeleton and the extracellular matrix, exocytosis, endocytosis, lateral compartmentalization, homotypic and heterotypic interactions between organelles, intercellular recognition and communication, host defense, as well as the specificity and flexibility of signaling pathways are among the issues of interest in this Special Issue. Membrane-bound organelles, such as exosomes, which circulate in the extracellular space and affect the immune status of distal recipient cells through their RNA, DNA, protein, and lipid cargo, have attracted intense scientific interest. These membranes and their synthetic analogues are being considered as appropriate vehicles for drug delivery in several diseases. Finally, within the scope of this issue is the presentation of advanced techniques that permit the study of dynamic interaction of biomembrane constituents.

Dr. Marilena Lekka
Dr. George Leondaritis
Guest Editors

Manuscript Submission Information

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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. Membranes 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.

Published Papers (3 papers)

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Research

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15 pages, 2211 KiB  
Article
Mitochondria Isolated from Hearts Subjected to Ischemia/Reperfusion Benefit from Adenine Nucleotide Translocase 1 Overexpression
by Andrea Dörner, Oleg Lynetskiy, Gerhild Euler, Ulf Landmesser, Klaus-Dieter Schlüter and Jacqueline Heger
Membranes 2021, 11(11), 836; https://doi.org/10.3390/membranes11110836 - 29 Oct 2021
Cited by 4 | Viewed by 1867
Abstract
Reperfusion is the only feasible therapy following myocardial infarction, but reperfusion has been shown to damage mitochondrial function and disrupt energy production in the heart. Adenine nucleotide translocase 1 (ANT1) facilitates the transfer of ADP/ATP across the inner mitochondrial membrane; therefore, we tested [...] Read more.
Reperfusion is the only feasible therapy following myocardial infarction, but reperfusion has been shown to damage mitochondrial function and disrupt energy production in the heart. Adenine nucleotide translocase 1 (ANT1) facilitates the transfer of ADP/ATP across the inner mitochondrial membrane; therefore, we tested whether ANT1 exerts protective effects on mitochondrial function during ischemia/reperfusion (I/R). The hearts of wild-type (WT) and transgenic ANT1-overexpressing (ANT1-TG) rats were exposed to I/R injury using the standard Langendorff technique, after which mitochondrial function, hemodynamic parameters, infarct size, and components of the contractile apparatus were determined. ANT1-TG hearts expressed higher ANT protein levels, with reduced levels of oxidative 4-hydroxynonenal ANT modifications following I/R. ANT1-TG mitochondria isolated from I/R hearts displayed stable calcium retention capacity (CRC) and improved membrane potential stability compared with WT mitochondria. Mitochondria isolated from ANT1-TG hearts experienced less restricted oxygen consumption than WT mitochondria after I/R. Left ventricular diastolic pressure (Pdia) decreased in ANT1-TG hearts compared with WT hearts following I/R. Preserved diastolic function was accompanied by a decrease in the phospho-lamban (PLB)/sarcoplasmic reticulum calcium ATPase (SERCA2a) ratio in ANT1-TG hearts compared with that in WT hearts. In addition, the phosphorylated (P)-PLB/PLB ratio increased in ANT1-TG hearts after I/R but not in WT hearts, which indicated more effective calcium uptake into the sarcoplasmic reticulum in ANT1-TG hearts. In conclusion, ANT1-TG rat hearts coped more efficiently with I/R than WT rat hearts, which was reflected by preserved mitochondrial energy balance, diastolic function, and calcium dynamics after reperfusion. Full article
(This article belongs to the Special Issue Biomembranes and Cell Signaling in Health and Disease)
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19 pages, 24287 KiB  
Article
Red Blood Cell Proteasome in Beta-Thalassemia Trait: Topology of Activity and Networking in Blood Bank Conditions
by Alkmini T. Anastasiadi, Vassilis L. Tzounakas, Vasiliki-Zoi Arvaniti, Monika Dzieciatkowska, Konstantinos Stamoulis, Marilena E. Lekka, Issidora S. Papassideri, Angelo D’Alessandro, Anastasios G. Kriebardis and Marianna H. Antonelou
Membranes 2021, 11(9), 716; https://doi.org/10.3390/membranes11090716 - 17 Sep 2021
Cited by 11 | Viewed by 2826
Abstract
Proteasomes are multi-catalytic complexes with important roles in protein control. Their activity in stored red blood cells (RBCs) is affected by both storage time and the donor’s characteristics. However, apart from their abundancy in the membrane proteome, not much is known about their [...] Read more.
Proteasomes are multi-catalytic complexes with important roles in protein control. Their activity in stored red blood cells (RBCs) is affected by both storage time and the donor’s characteristics. However, apart from their abundancy in the membrane proteome, not much is known about their topology, activity, and networking during the storage of RBCs from beta-thalassemia trait donors (βThal+). For this purpose, RBC units from fourteen βThal+ donors were fractionated and studied for proteasome activity distribution and interactome through fluorometric and correlation analyses against units of sex- and aged-matched controls. In all the samples examined, we observed a time-dependent translocation and/or activation of the proteasome in the membrane and a tight connection of activity with the oxidative burden of cells. Proteasomes were more active in the βThal+ membranes and supernatants, while the early storage networking of 20S core particles and activities showed a higher degree of connectivity with chaperones, calpains, and peroxiredoxins, which were nonetheless present in all interactomes. Moreover, the βThal+ interactomes were specially enriched in kinases, metabolic enzymes, and proteins differentially expressed in βThal+ membrane, including arginase-1, piezo-1, and phospholipid scramblase. Overall, it seems that βThal+ erythrocytes maintain a considerable “proteo-vigilance” during storage, which is closely connected to their distinct antioxidant dynamics and membrane protein profile. Full article
(This article belongs to the Special Issue Biomembranes and Cell Signaling in Health and Disease)
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Review

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18 pages, 758 KiB  
Review
p53 Signaling on Microenvironment and Its Contribution to Tissue Chemoresistance
by Leonel Cardozo de Menezes e Souza, Anderson Faletti, Carla Pires Veríssimo, Mariana Paranhos Stelling and Helena Lobo Borges
Membranes 2022, 12(2), 202; https://doi.org/10.3390/membranes12020202 - 09 Feb 2022
Cited by 9 | Viewed by 2133
Abstract
Chemoresistance persists as a significant, unresolved clinical challenge in many cancer types. The tumor microenvironment, in which cancer cells reside and interact with non-cancer cells and tissue structures, has a known role in promoting every aspect of tumor progression, including chemoresistance. However, the [...] Read more.
Chemoresistance persists as a significant, unresolved clinical challenge in many cancer types. The tumor microenvironment, in which cancer cells reside and interact with non-cancer cells and tissue structures, has a known role in promoting every aspect of tumor progression, including chemoresistance. However, the molecular determinants of microenvironment-driven chemoresistance are mainly unknown. In this review, we propose that the TP53 tumor suppressor, found mutant in over half of human cancers, is a crucial regulator of cancer cell-microenvironment crosstalk and a prime candidate for the investigation of microenvironment-specific modulators of chemoresistance. Wild-type p53 controls the secretion of factors that inhibit the tumor microenvironment, whereas altered secretion or mutant p53 interfere with p53 function to promote chemoresistance. We highlight resistance mechanisms promoted by mutant p53 and enforced by the microenvironment, such as extracellular matrix remodeling and adaptation to hypoxia. Alterations of wild-type p53 extracellular function may create a cascade of spatial amplification loops in the tumor tissue that can influence cellular behavior far from the initial oncogenic mutation. We discuss the concept of chemoresistance as a multicellular/tissue-level process rather than intrinsically cellular. Targeting p53-dependent crosstalk mechanisms between cancer cells and components of the tumor environment might disrupt the waves of chemoresistance that spread across the tumor tissue, increasing the efficacy of chemotherapeutic agents. Full article
(This article belongs to the Special Issue Biomembranes and Cell Signaling in Health and Disease)
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