title: Role of calcium channels in the protective effect of hydrogen sulfide in rat cardiomyoblasts.
abstract: BACKGROUND
  Hydrogen sulfide contributes to the reduction of oxidative stress-related injury in cardiomyocytes but the underlying mechanism is still unclear.
  
  
  OBJECTIVE
  Here we investigated the role of voltage-operated calcium channels (VOCCs) as mediators of the beneficial effect of H2S against oxidative stress in cultured rat cardiomyoblasts (H9c2).
  
  
  METHODS
  Intracellular calcium signals were measured by fluorimetric live cell imaging and cell viability by colorimetric assay.
  
  
  RESULTS
  Treatment with H2S donor (NaHS 10 µM) or Nifedipine (10 µM) decreased resting intracellular calcium concentration [Ca]i, suggesting that L-type VOCCs are negatively modulated by H2S. In the presence of Nifedipine H2S was still able to lower [Ca]i, while co-incubation with Nifedipine and Ni(2+) 100 µM completely prevented H2S-dependent [Ca]i decrease, suggesting that both L-type and T-type VOCCs are inhibited by H2S. In addition, in the same experimental conditions, H2S triggered a slow increase of [Ca]i whose molecular nature remains to be clarified. Pretreatment of H9c2 with NaHS (10 µM) significantly prevented cell death induced by H2O2. This effect was mimicked by pretreatment with L-Type calcium channel inhibitor Nifedipine (10 µM).
  
  
  CONCLUSIONS
  The data provide the first evidence that H2S protects rat cardiomyoblasts against oxidative challenge through the inhibition of L-type calcium channels.
authors.affiliation: Department of Life Sciences and Systems Biology, University of Torino, Torino, Italy.
authors.forename: Daniele
authors.initials: D
authors.lastname: Avanzato
authors.forename: Annalisa
authors.initials: A
authors.lastname: Merlino
authors.forename: Sabina
authors.initials: S
authors.lastname: Porrera
authors.forename: Rui
authors.initials: R
authors.lastname: Wang
authors.forename: Luca
authors.initials: L
authors.lastname: Munaron
authors.forename: Daniele
authors.initials: D
authors.lastname: Mancardi
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000737:chemistry / Q000378:metabolism*; D020747:Calcium Channels, T-Type / Q000737:chemistry / Q000378:metabolism*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000633:toxicity; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D013440:Sulfides / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D020747:Calcium Channels, T-Type; D013440:Sulfides; D006861:Hydrogen Peroxide; C025451:sodium bisulfide; D009543:Nifedipine; D002118:Calcium; D006862:Hydrogen Sulfide