Hydrogen sulfide donor NaHS induces death of alveolar epithelial L2 cells that is associated with cellular shrinkage, transgelin expression and myosin phosphorylation

• Fujii Yusuke

  Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

• Funakoshi Takeshi

  Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

• Unuma Kana

  Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

• Noritake Kanako

  Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

• Aki Toshihiko

  Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

• Uemura Koichi

  Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

Abstract

Hydrogen sulfide (H₂S) is a highly toxic gaseous molecule that causes death to humans exposed to high concentrations. H₂S is absorbed into the body through the alveolar epithelium and other tissues. The aim of this study is to evaluate the molecular mechanism underling acute lung injury caused by the inhalation of high concentrations of H₂S. Rat lung epithelium-derived L2 cells were exposed to a H₂S donor, NaHS, at concentrations of 2-4 mM for 1-6 hr. NaHS caused shrinkage and death of the cells without caspase activation. An actin-binding protein, transgelin, was identified as one of the NaHS-inducible proteins in the cells. NaHS increased myosin light chain (MLC) phosphorylation, indicating that actomyosin-mediated cellular contractility and/or motility could be increased after NaHS exposure. The administration of ML-7, a myosin light chain kinase (MLCK) inhibitor, accelerated cell death after NaHS exposure. Based on these data, we conclude that the increase in MLC phosphorylation in response to NaHS exposure is a cellular protective reaction against NaHS toxicity. Enhancements in smooth muscle cell properties such as transgelin expression and actomyosin-mediated contractility/motility might be involved in cell survival after NaHS exposure.

Journal

• The Journal of Toxicological Sciences

  The Journal of Toxicological Sciences 41 (5), 645-654, 2016

  The Japanese Society of Toxicology

Keywords

• Hydrogen sulfide
• L2 cells
• Transgelin
• Myosin light chain kinase

Details

• CRID: 1390001204903433856
• NII Article ID: 130005266228
• NII Book ID: AN00002808
• DOI: 10.2131/jts.41.645
• ISSN: 18803989
• ISSN: 03881350
• NDL BIB ID: 027712130
• PubMed: 27665774
• Web Site: http://id.ndl.go.jp/bib/027712130
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I027712130
• Web Site: https://www.jstage.jst.go.jp/article/jts/41/5/41_645/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2017224986
• Text Lang: en
• Data Source:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed