Extracellular Vesicles in Inflammation and Inflammatory Diseases

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 4258

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: 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
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E-Mail Website
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; alcohol-associated liver disease; innate immunity; antigen presentation; proteasome; protein posttranslational modifications; animal models for a hepatitis study; long-acting drugs
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.

Dr. Raghubendra S. Dagur
Prof. Dr. Natalia Osna
Dr. Guoku Hu
Guest Editors

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Keywords

  • Extracellular vesicles
  • Exosomes
  • Apoptotic bodies
  • Macrovesicles
  • Exomere
  • Ectosomes
  • Inflammation
  • Inflammatory diseases

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Published Papers (1 paper)

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Research

18 pages, 2790 KiB  
Article
Alcohol-and-HIV-Induced Lysosomal Dysfunction Regulates Extracellular Vesicles Secretion in Vitro and in Liver-Humanized Mice
by Raghubendra Singh Dagur, Moses New-Aaron, Murali Ganesan, Weimin Wang, Svetlana Romanova, Srivatsan Kidambi, Kusum K. Kharbanda, Larisa Y. Poluektova and Natalia A. Osna
Biology 2021, 10(1), 29; https://doi.org/10.3390/biology10010029 - 5 Jan 2021
Cited by 13 | Viewed by 3309
Abstract
Background: Alcohol abuse is common in people living with HIV-1 and dramatically
enhances the severity of HIV-induced liver damage by inducing oxidative stress and lysosomal
dysfunction in the liver cells. We hypothesize that the increased release of extracellular vesicles
(EVs) in hepatocytes and [...] Read more.
Background: Alcohol abuse is common in people living with HIV-1 and dramatically
enhances the severity of HIV-induced liver damage by inducing oxidative stress and lysosomal
dysfunction in the liver cells. We hypothesize that the increased release of extracellular vesicles
(EVs) in hepatocytes and liver humanized mouse model is linked to lysosome dysfunction. Methods:
The study was performed on primary human hepatocytes and human hepatoma RLWXP-GFP (Huh
7.5 cells stably transfected with CYP2E1 and XPack-GFP) cells and validated on ethanol-fed liverhumanized
fumarylacetoacetate hydrolase (Fah)-/-, Rag2-/-, common cytokine receptor gamma chain
knockout (FRG-KO) mice. Cells and mice were infected with HIV-1ADA virus. Results: We observed
an increase in the secretion of EVs associated with a decrease in lysosomal activity and expression
of lysosomal-associated membrane protein 1. Next-generation RNA sequencing of primary human
hepatocytes revealed 63 differentially expressed genes, with 13 downregulated and 50 upregulated
genes in the alcohol–HIV-treated group. Upstream regulator analysis of differentially expressed
genes through Ingenuity Pathway Analysis identified transcriptional regulators affecting downstream
genes associated with increased oxidative stress, lysosomal associated disease, and function and
EVs biogenesis. Our in vitro findings were corroborated by in vivo studies on human hepatocytetransplanted
humanized mice, indicating that intensive EVs’ generation by human hepatocytes and
their secretion to serum was associated with increased oxidative stress and reduction in lysosomal
activities triggered by HIV infection and ethanol diet. Conclusion: HIV-and-ethanol-metabolisminduced
EVs release is tightly controlled by lysosome status in hepatocytes and participates in the
development of double-insult-induced liver injury. Full article
(This article belongs to the Special Issue Extracellular Vesicles in Inflammation and Inflammatory Diseases)
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