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8.3
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Journals
Biomolecules
Special Issues
Molecular Research on Airway Diseases
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Molecular Research on Airway Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (1 December 2023) | Viewed by 1394

Special Issue Editor

Prof. Dr. Ken Ohta

E-Mail Website
Guest Editor
Anti-Tuberculosis Association (JATA), Fukujuji Hospital, Tokyo, Japan
Interests: asthma; COPD; interstitial lung disease

Special Issue Information

Dear Colleagues,

The development of basic research has made it possible to clarify the molecular mechanisms of various airway diseases. In this Special Issue entitled “Molecular Research on Airway Diseases”, we would like to focus on asthma, COPD and interstitial lung disease. There are a variety of ways to identify molecules involved in pathological conditions. The results of cell and molecular biology have provided a lot of hints for identifying molecules playing a pivotal role in a disease, and their involvement could be confirmed functionally by employing appropriate animal models and in the real world in humans by revealing their existence in the human specimens obtained from individuals suffering from a corresponding airway disease. The identification of the molecules involved could bring about a new therapeutic strategy or preventive approach as can be seen in the field of asthma in which various biological agents target identified molecules. Their efficacy could provide the real position of the target for the biological agent in the pathogenesis of the disease condition and could allow us to observe close relationships between molecules and clinical phenotypes. Moreover, the identified molecules could be good biomarkers for diagnosing a disease or assessing the condition of a disease as well as analyzing endotypes of airway diseases by means of the cluster analysis.

We look forward to reading your contribution.

Prof. Dr. Ken Ohta
Guest Editor

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. Biomolecules 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

  • asthma
  • COPD
  • interstitial lung disease
  • cell biology
  • animal models
  • therapeutic strategy
  • biomarker
  • endotype
  • cluster analysis

Published Papers (1 paper)

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Research

15 pages, 7817 KiB  
Article
Extracellular Acetylated Histone 3.3 Induces Inflammation and Lung Tissue Damage
by Mario C. Rico, Oscar Perez-Leal, Mary F. Barbe, Mamta Amin, Dennis J. Colussi, Magda L. Florez, Victor Olusajo, Dennise S. Rios and Carlos A. Barrero
Biomolecules 2023, 13(9), 1334; https://doi.org/10.3390/biom13091334 - 31 Aug 2023
Viewed by 963
Abstract
Extracellular histones, part of the protein group known as damage-associated molecular patterns (DAMPs), are released from damaged or dying cells and can instigate cellular toxicity. Within the context of chronic obstructive pulmonary disease (COPD), there is an observed abundance of extracellular histone H3.3, [...] Read more.
Extracellular histones, part of the protein group known as damage-associated molecular patterns (DAMPs), are released from damaged or dying cells and can instigate cellular toxicity. Within the context of chronic obstructive pulmonary disease (COPD), there is an observed abundance of extracellular histone H3.3, indicating potential pathogenic implications. Notably, histone H3.3 is often found hyperacetylated (AcH3.3) in the lungs of COPD patients. Despite these observations, the specific role of these acetylated histones in inducing pulmonary tissue damage in COPD remains unclear. To investigate AcH3.3’s impact on lung tissue, we administered recombinant histones (rH2A, rH3.3, and rAcH3.3) or vehicle solution to mice via intratracheal instillation. After 48 h, we evaluated the lung toxicity damage and found that the rAcH3.3 treated animals exhibited more severe lung tissue damage compared to those treated with non-acetylated H3.3 and controls. The rAcH3.3 instillation resulted in significant histological changes, including alveolar wall rupture, epithelial cell damage, and immune cell infiltration. Micro-CT analysis confirmed macroscopic structural changes. The rAcH3.3 instillation also increased apoptotic activity (cleavage of caspase 3 and 9) and triggered acute systemic inflammatory marker activation (TNF-α, IL-6, MCP-3, or CXCL-1) in plasma, accompanied by leukocytosis and lymphocytosis. Confocal imaging analysis confirmed lymphocytic and monocytic/macrophage lung infiltration in response to H3.3 and AcH3.3 administration. Taken together, our findings implicate extracellular AcH3.3 in inducing cytotoxicity and acute inflammatory responses, suggesting its potential role in promoting COPD-related lung damage progression. Full article
(This article belongs to the Special Issue Molecular Research on Airway Diseases)
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