Involvement of redox-signalling in endogenous hydrogen sulfide production

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Recently, cystathionine-Iγ-lyase (CSE) was found to provide the major physiological pathway for H2S, the third member of the gasotransmitter family. In various pathophysiological conditions, H2S exerted protective effects based on its antioxidant, anti-inflammatory, anti-hypertensive and other regulatory functions. Interestingly, CSE expression had been only poorly studied and only in relation with inflammatory processes. Therefore, the study by Hassan et al. in this issue of the BJP, provides a considerable advance by furnishing direct experimental evidence for the involvement of redox signalling in the regulation of CSE gene expression. They found that PDGF up-regulated CSE expression and activity that was abolished by antioxidants and by deletion of the transcription factor nuclear erythroid-2-related factor-2 (Nrf2). Furthermore, PDGF induced Nrf2 binding to its consensus sequence that was again reversed by antioxidants. As Nrf2 also governs CO biosynthesis, and PDGF inversely affects H2S and NO production, these data could indicate a concerted regulation of the three gasotransmitters by redox signalling.

Original languageEnglish
Pages (from-to)2228-2230
Number of pages3
JournalBritish Journal of Pharmacology
Volume166
Issue number8
DOIs
Publication statusPublished - Aug 2012

Fingerprint

Cystathionine
Hydrogen Sulfide
Lyases
Oxidation-Reduction
Gasotransmitters
Antioxidants
NF-E2 Transcription Factor
Consensus Sequence
Carbon Monoxide
Antihypertensive Agents
Anti-Inflammatory Agents
Gene Expression

Keywords

  • cystathionine-Iγ-lyase
  • gasotransmitters
  • hydrogen sulfide
  • nuclear erythroid-2-related factor-2
  • PDGF
  • redox signalling

ASJC Scopus subject areas

  • Pharmacology

Cite this

Involvement of redox-signalling in endogenous hydrogen sulfide production. / Gallyas, F.

In: British Journal of Pharmacology, Vol. 166, No. 8, 08.2012, p. 2228-2230.

Research output: Contribution to journalArticle

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