Extracellular Vesicles in Inflammation and Inflammatory Diseases Edition 2.0

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (30 March 2022) | Viewed by 14244

Special Issue Editors


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Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Veteran Affairs Medical Center, 4101 Woolworth Ave, R151, Omaha, NE 68105-8080, USA
Interests: hepatitis C, B, HIV and other viral hepatitis; alcoholic liver disease; innate immunity; antigen presentation; proteasome; protein posttranslational modifications; animal models for hepatitis study
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Veteran Affairs Medical Center, 4101 Woolworth Ave, R151, Omaha, NE 68105-8080, USA
Interests: cellular and molecular mechanisms of extracellular vesicles (EVs) biogenesis; HIV-associated alcoholic liver disease and neuropathogenesis; EVs as biomarkers and therapeutics; HIV and immunogenicity; HIV-1, HBV and HCV mono- and coinfections; humanized mouse models; alcoholic and non-alcoholic liver diseases
Special Issues, Collections and Topics in MDPI journals
Department of Pharmacology & Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198-5880, USA
Interests: HIV and drug abuse synergy; exosomes; noncoding RNAs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Extracellular vesicles (EVs) have a pivotal role in inflammation, and EVs including exosomes, apoptotic bodies, and microvesicles show significant alteration in people who are on drugs of abuse (e.g., cocaine, alcohol, opioids) and in those with inflammatory diseases (e.g., gastrointestinal inflammation, liver diseases, autoimmune, neuroinflammation). EVs are released by all cell types and have a prominent role in the maintenance of cell homeostasis and intercellular communication. EVs regulate cell-intrinsic functions and cell–cell communication by removing or transferring their cargo of miRNAs, RNAs, lncRNAs, circRNA, cytokines, proteins, and lipids to extracellular milieus or in recipient cells. As alteration in the number of EVs and cargo is disease specific, EVs have therapeutic potential and could be used as biomarkers for inflammation and other inflammatory diseases.

For this Special Issue, we encourage the submission of manuscripts on any aspect of extracellular vesicles, including but not limited to the role of extracellular vesicles in disease pathogenesis; biogenesis; intercellular or interorgan communication; biomarkers and therapeutics; proteomics, lipidomics, and metabolomics of EVs; drugs of abuse; inflammatory diseases; etc. We accept reviews, conference proceedings, and short- and full-size research papers which cover the subjects as mentioned above.

Prof. Dr. Natalia Osna
Dr. Raghubendra S. Dagur
Dr. Guoku Hu
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. Biology 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

  • extracellular vesicles
  • exosomes
  • apoptotic bodies
  • macrovesicles
  • exomere
  • ectosomes
  • inflammation
  • inflammatory diseases

Published Papers (4 papers)

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Research

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19 pages, 4773 KiB  
Article
Long Noncoding RNA GAS5 Contained in Exosomes Derived from Human Adipose Stem Cells Promotes Repair and Modulates Inflammation in a Chronic Dermal Wound Healing Model
by Rekha S. Patel, Sabrina Impreso, Ashley Lui, Gitanjali Vidyarthi, Paul Albear and Niketa A. Patel
Biology 2022, 11(3), 426; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11030426 - 11 Mar 2022
Cited by 15 | Viewed by 2794
Abstract
Chronic recalcitrant wounds result from delayed or slowed healing processes. Underlying inflammation is a substantial risk factor for impaired dermal wound healing and often leads to chronic wound-related sequelae. Human adipose stem cells (hASCs) have shown tremendous potential in regenerative medicine. The goal [...] Read more.
Chronic recalcitrant wounds result from delayed or slowed healing processes. Underlying inflammation is a substantial risk factor for impaired dermal wound healing and often leads to chronic wound-related sequelae. Human adipose stem cells (hASCs) have shown tremendous potential in regenerative medicine. The goal of this project was to improve the outcome of chronic wounds by harvesting the exosomes from hASCs for therapeutic intervention. The results demonstrate that long noncoding RNA GAS5 is highly enriched in hASC exosomes and, further, that GAS5 is central to promoting wound repair in vitro. To evaluate the outcome of wound healing in a chronic low-grade inflammatory environment, lipopolysaccharide-treated HDF cells were evaluated for their response to hASC exosome treatment. Ingenuity pathway analysis identified inflammation pathways and genes affected by exosomes in a GAS5-dependent manner. Using siRNA to deplete GAS5 in HDF, the results demonstrated that Toll-like receptor 7 (TLR7) expression levels were regulated by GAS5. Importantly, the results demonstrate that GAS5 regulates inflammatory pathway genes in a chronic inflammation environment. The results presented here demonstrate that hASC exosomes are a viable therapeutic that accelerate the healing of chronic recalcitrant wounds. Full article
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12 pages, 2776 KiB  
Article
Proteomic Analysis of Exosomes Secreted from Human Alpha-1 Antitrypsin Overexpressing Mesenchymal Stromal Cells
by Hua Wei, Erica Green, Lauren Ball, Hongkuan Fan, Jennifer Lee, Charlie Strange and Hongjun Wang
Biology 2022, 11(1), 9; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11010009 - 21 Dec 2021
Cited by 4 | Viewed by 3344
Abstract
Extracellular vesicles (EVs) mediate many therapeutic effects of stem cells during cellular therapies. Bone marrow-derived mesenchymal stromal cells (BM-MSCs) were manufactured to overexpress the human antiprotease alpha-1 antitrypsin (hAAT) and studied to compare the EV production compared to lentivirus treated control MSCs. The [...] Read more.
Extracellular vesicles (EVs) mediate many therapeutic effects of stem cells during cellular therapies. Bone marrow-derived mesenchymal stromal cells (BM-MSCs) were manufactured to overexpress the human antiprotease alpha-1 antitrypsin (hAAT) and studied to compare the EV production compared to lentivirus treated control MSCs. The goal of this study was to compare protein profiles in the EVs/exosomes of control and hAAT-MSCs using unbiased, high resolution liquid chromatography and mass spectrometry to explore differences. Nanoparticle tracking analysis (NTA) showed that the particle size of the EVs from control MSCs or hAAT-MSCs ranged from 30 to 200 nm. Both MSCs and hAAT-MSCs expressed exosome-associated proteins, including CD63, CD81, and CD9. hAAT-MSCs also expressed high levels of hAAT. We next performed proteomic analysis of EVs from three healthy donor cell lines. Exosomes collected from cell supernatant were classified by GO analysis which showed proteins important to cell adhesion and extracellular matrix organization. However, there were differences between exosomes from control MSCs and hAAT-MSCs in cytokine signaling of the immune system, stem cell differentiation, and carbohydrate metabolism (p < 0.05). These results show that hAAT-MSC exosomes contain a different profile of paracrine effectors with altered immune function, impacts on MSC stemness, differentiation, and prevention of cell apoptosis and survival that could contribute to improved therapeutic functions. Full article
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20 pages, 4666 KiB  
Article
Virus Mimetic Poly (I:C)-Primed Airway Exosome-like Particles Enter Brain and Induce Inflammatory Cytokines and Mitochondrial Reactive Oxygen Species in Microglia
by Deimantė Kulakauskienė, Deimantė Narauskaitė, Dovydas Gečys, Otilija Juknaitė, Lina Jankauskaitė, Aistė Masaitytė, Jurgita Šventoraitienė, Hermanas Inokaitis, Zoja Miknienė, Ilona Sadauskienė, Giedrius Steponaitis, Zbigniev Balion, Ramunė Morkūnienė, Neringa Paužienė, Dainius Haroldas Pauža and Aistė Jekabsone
Biology 2021, 10(12), 1359; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10121359 - 20 Dec 2021
Cited by 3 | Viewed by 4839
Abstract
Viral infections induce extracellular vesicles (EVs) containing viral material and inflammatory factors. Exosomes can easily cross the blood-brain barrier during respiratory tract infection and transmit the inflammatory signal to the brain; however, such a hypothesis has no experimental evidence. The study investigated whether [...] Read more.
Viral infections induce extracellular vesicles (EVs) containing viral material and inflammatory factors. Exosomes can easily cross the blood-brain barrier during respiratory tract infection and transmit the inflammatory signal to the brain; however, such a hypothesis has no experimental evidence. The study investigated whether exosome-like vesicles (ELVs) from virus mimetic poly (I:C)-primed airway cells enter the brain and interact with brain immune cells microglia. Airway cells were isolated from Wistar rats and BALB/c mice; microglial cell cultures—from Wistar rats. ELVs from poly (I:C)-stimulated airway cell culture medium were isolated by precipitation, visualised by transmission electron microscopy, and evaluated by nanoparticle analyser; exosomal markers CD81 and CD9 were determined by ELISA. For in vitro and in vivo tracking, particles were loaded with Alexa Fluor 555-labelled RNA. Intracellular reactive oxygen species (ROS) were evaluated by DCFDA fluorescence and mitochondrial superoxide—by MitoSOX. ELVs from poly (I:C)-primed airway cells entered the brain within an hour after intranasal introduction, were internalised by microglia and induced intracellular and intramitochondrial ROS production. There was no ROS increase in microglial cells was after treatment with ELVs from airway cells untreated with poly (I:C). In addition, poly (I:C)-primed airway cells induced inflammatory cytokine expression in the brain. The data indicate that ELVs secreted by virus-primed airway cells might enter the brain, cause the activation of microglial cells and neuroinflammation. Full article
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Review

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23 pages, 798 KiB  
Review
Pathological Contribution of Extracellular Vesicles and Their MicroRNAs to Progression of Chronic Liver Disease
by Chanbin Lee, Jinsol Han and Youngmi Jung
Biology 2022, 11(5), 637; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11050637 - 21 Apr 2022
Cited by 7 | Viewed by 2481
Abstract
Extracellular vesicles (EVs) are membrane-bound endogenous nanoparticles released by the majority of cells into the extracellular space. Because EVs carry various cargo (protein, lipid, and nucleic acids), they transfer bioinformation that reflects the state of donor cells to recipient cells both in healthy [...] Read more.
Extracellular vesicles (EVs) are membrane-bound endogenous nanoparticles released by the majority of cells into the extracellular space. Because EVs carry various cargo (protein, lipid, and nucleic acids), they transfer bioinformation that reflects the state of donor cells to recipient cells both in healthy and pathologic conditions, such as liver disease. Chronic liver disease (CLD) affects numerous people worldwide and has a high mortality rate. EVs released from damaged hepatic cells are involved in CLD progression by impacting intercellular communication between EV-producing and EV-receiving cells, thereby inducing a disease-favorable microenvironment. In patients with CLD, as well as in the animal models of CLD, the levels of released EVs are elevated. Furthermore, these EVs contain high levels of factors that accelerate disease progression. Therefore, it is important to understand the diverse roles of EVs and their cargoes to treat CLD. Herein, we briefly explain the biogenesis and types of EVs and summarize current findings presenting the role of EVs in the pathogenesis of CLD. As the role of microRNAs (miRNAs) within EVs in liver disease is well documented, the effects of miRNAs detected in EVs on CLD are reviewed. In addition, we discuss the therapeutic potential of EVs to treat CLD. Full article
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