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Hydrogen Sulfide: A Novel Player in Airway Development, Pathophysiology of Respiratory Diseases, and Antiviral Defenses.
Am J Respir Cell Mol Biol. 2017 10; 57(4):403-410.AJ

Abstract

Hydrogen sulfide (H2S) is a biologically relevant signaling molecule in mammals. Along with the volatile substances nitric oxide (NO) and carbon monoxide (CO), H2S is defined as a gasotransmitter. It plays a physiological role in a variety of functions, including synaptic transmission, vascular tone, angiogenesis, inflammation, and cellular signaling. The generation of H2S is catalyzed by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST). The expression of CBS and CSE is tissue specific, with CBS being expressed predominantly in the brain, and CSE in peripheral tissues, including lungs. CSE expression and activity are developmentally regulated, and recent studies suggest that CSE plays an important role in lung alveolarization during fetal development. In the respiratory tract, endogenous H2S has been shown to participate in the regulation of important functions such as airway tone, pulmonary circulation, cell proliferation or apoptosis, fibrosis, oxidative stress, and inflammation. In the past few years, changes in the generation of H2S have been linked to the pathogenesis of a variety of acute and chronic inflammatory lung diseases, including asthma and chronic obstructive pulmonary disease. Recently, our laboratory made the critical discovery that cellular H2S exerts broad-spectrum antiviral activity both in vitro and in vivo, in addition to independent antiinflammatory activity. These findings have important implications for the development of novel therapeutic strategies for viral respiratory infections, as well as other inflammatory lung diseases, especially in light of recent significant efforts to generate controlled-release H2S donors for clinical therapeutic applications.

Authors+Show Affiliations

Departments of 1 Pediatrics and.2 Microbiology and Immunology, and.Departments of 1 Pediatrics and.Departments of 1 Pediatrics and. 2 Microbiology and Immunology, and. 3 Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston, Texas.Departments of 1 Pediatrics and. 2 Microbiology and Immunology, and. 3 Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston, Texas.

Pub Type(s)

Journal Article
Review
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28481637

Citation

Bazhanov, Nikolay, et al. "Hydrogen Sulfide: a Novel Player in Airway Development, Pathophysiology of Respiratory Diseases, and Antiviral Defenses." American Journal of Respiratory Cell and Molecular Biology, vol. 57, no. 4, 2017, pp. 403-410.
Bazhanov N, Ansar M, Ivanciuc T, et al. Hydrogen Sulfide: A Novel Player in Airway Development, Pathophysiology of Respiratory Diseases, and Antiviral Defenses. Am J Respir Cell Mol Biol. 2017;57(4):403-410.
Bazhanov, N., Ansar, M., Ivanciuc, T., Garofalo, R. P., & Casola, A. (2017). Hydrogen Sulfide: A Novel Player in Airway Development, Pathophysiology of Respiratory Diseases, and Antiviral Defenses. American Journal of Respiratory Cell and Molecular Biology, 57(4), 403-410. https://doi.org/10.1165/rcmb.2017-0114TR
Bazhanov N, et al. Hydrogen Sulfide: a Novel Player in Airway Development, Pathophysiology of Respiratory Diseases, and Antiviral Defenses. Am J Respir Cell Mol Biol. 2017;57(4):403-410. PubMed PMID: 28481637.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen Sulfide: A Novel Player in Airway Development, Pathophysiology of Respiratory Diseases, and Antiviral Defenses. AU - Bazhanov,Nikolay, AU - Ansar,Maria, AU - Ivanciuc,Teodora, AU - Garofalo,Roberto P, AU - Casola,Antonella, PY - 2017/5/10/pubmed PY - 2017/10/6/medline PY - 2017/5/9/entrez KW - H2S donors KW - antiviral KW - hydrogen sulfide SP - 403 EP - 410 JF - American journal of respiratory cell and molecular biology JO - Am J Respir Cell Mol Biol VL - 57 IS - 4 N2 - Hydrogen sulfide (H2S) is a biologically relevant signaling molecule in mammals. Along with the volatile substances nitric oxide (NO) and carbon monoxide (CO), H2S is defined as a gasotransmitter. It plays a physiological role in a variety of functions, including synaptic transmission, vascular tone, angiogenesis, inflammation, and cellular signaling. The generation of H2S is catalyzed by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST). The expression of CBS and CSE is tissue specific, with CBS being expressed predominantly in the brain, and CSE in peripheral tissues, including lungs. CSE expression and activity are developmentally regulated, and recent studies suggest that CSE plays an important role in lung alveolarization during fetal development. In the respiratory tract, endogenous H2S has been shown to participate in the regulation of important functions such as airway tone, pulmonary circulation, cell proliferation or apoptosis, fibrosis, oxidative stress, and inflammation. In the past few years, changes in the generation of H2S have been linked to the pathogenesis of a variety of acute and chronic inflammatory lung diseases, including asthma and chronic obstructive pulmonary disease. Recently, our laboratory made the critical discovery that cellular H2S exerts broad-spectrum antiviral activity both in vitro and in vivo, in addition to independent antiinflammatory activity. These findings have important implications for the development of novel therapeutic strategies for viral respiratory infections, as well as other inflammatory lung diseases, especially in light of recent significant efforts to generate controlled-release H2S donors for clinical therapeutic applications. SN - 1535-4989 UR - https://www.unboundmedicine.com/medline/citation/28481637/Hydrogen_Sulfide:_A_Novel_Player_in_Airway_Development_Pathophysiology_of_Respiratory_Diseases_and_Antiviral_Defenses_ L2 - https://www.atsjournals.org/doi/10.1165/rcmb.2017-0114TR?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -