ArticlePloS one2014
Hydrogen sulfide inhibits formaldehyde-induced endoplasmic reticulum stress in PC12 cells by upregulation of SIRT-1.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 72 citations in OpenAlex.
- Hydrogen sulfide donor NaHS inhibits formaldehyde-induced epithelial-mesenchymal transition in human lung epithelial cells via activating TGF-β1/Smad2/3 and MAPKs signaling pathways.Current research in toxicology · 2024Article
- Article
- HMolecular neurobiology · 2023Review
- Targeting Homocysteine and Hydrogen Sulfide Balance as Future Therapeutics in Cancer Treatment.Antioxidants (Basel, Switzerland) · 2023Review
- Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration.Molecular medicine reports · 2023Article
- The Impact of Drugs on Hydrogen Sulfide Homeostasis in Mammals.Antioxidants (Basel, Switzerland) · 2023Review
- Improvement of autophagic flux mediates the protection of hydrogen sulfide against arecoline-elicited neurotoxicity in PC12 cells.Cell cycle (Georgetown, Tex.) · 2022Article
- The Protective Effects of Hydrogen Sulfide New Donor MethylMolecules (Basel, Switzerland) · 2022Article
- Hydrogen Sulfide (HCurrent neuropharmacology · 2022Review
- Hydrogen sulfide-induced GAPDH sulfhydration disrupts the CCAR2-SIRT1 interaction to initiate autophagy.Autophagy · 2021Article
- Spatiotemporal regulation of hydrogen sulfide signaling in the kidney.Redox biology · 2021Review
- Hydrogen Sulfide and the Immune System.Advances in experimental medicine and biology · 2021Article
- RNA oxidation in chromatin modification and DNA-damage response following exposure to formaldehyde.Scientific reports · 2020Article
- Hydrogen Sulfide Plays an Important Protective Role through Influencing Endoplasmic Reticulum Stress in Diseases.International journal of biological sciences · 2020Review
- Hydrogen Sulfide Inhibits Formaldehyde-Induced Senescence in HT-22 Cells via Upregulation of Leptin Signaling.Neuromolecular medicine · 2019Article
- Restoration of skeletal muscle homeostasis by hydrogen sulfide during hyperhomocysteinemia-mediated oxidative/ER stress conditionCanadian journal of physiology and pharmacology · 2019Review
- Hydrogen Sulfide Inhibits High Glucose-Induced Neuronal Senescence by Improving Autophagic FluxFrontiers in molecular neuroscience · 2019Article
- Gasotransmitter hydrogen sulfide signaling in neuronal health and disease.Biochemical pharmacology · 2018Review
- Hydrogen Sulfide Inhibits Chronic Unpredictable Mild Stress-Induced Depressive-Like Behavior by Upregulation of Sirt-1: Involvement in Suppression of Hippocampal Endoplasmic Reticulum Stress.The international journal of neuropsychopharmacology · 2017Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFormaldehyde (FA), a well-known environmental pollutant, has been classified as a neurotoxic molecule. Our recent data demonstrate that hydrogen sulfide (H2S), the third gaseous transmitter, has a protective effect on the neurotoxicity of FA. However, the exact mechanisms underlying this protection remain largely unknown. Endoplasmic reticulum (ER) stress has been implicated in the neurotoxicity of FA. Silent mating type information regulator 2 homolog 1 (SIRT-1), a histone deacetylases, has various biological activities, including the extension of lifespan, the modulation of ER stress, and the neuroprotective action.
objectiveWe hypothesize that the protection of H2S against FA-induced neurotoxicity involves in inhibiting ER stress by upregulation of SIRT-1. The present study attempted to investigate the protective effect of H2S on FA-induced ER stress in PC12 cells and the contribution of SIRT-1 to the protection of H2S against FA-induced injuries, including ER stress, cytotoxicity and apoptosis. PRINCIPAL
findingsWe found that exogenous application of sodium hydrosulfide (NaHS; an H2S donor) significantly attenuated FA-induced ER stress responses, including the upregulated levels of glucose-regulated protein 78, C/EBP homologous protein, and cleaved caspase-12 expression. We showed that NaHS upregulates the expression of SIRT-1 in PC12 cells. Moreover, the protective effects of H2S on FA-elicited ER stress, cytotoxicity and apoptosis were reversed by Sirtinol, a specific inhibitor of SIRT-1. CONCLUSION/SIGNIFICANCE: These data indicate that H2S exerts its protection against the neurotoxicity of FA through overcoming ER stress via upregulation of SIRT-1. Our findings provide novel insights into the protective mechanisms of H2S against FA-induced neurotoxicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.