Role of Calcium Channels in the Protective Effect of Hydrogen Sulfide in Rat Cardiomyoblasts

• Main Authors: Daniele Avanzato, Annalisa Merlino, Sabina Porrera, Rui Wang, Luca Munaron, Daniele Mancardi
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2014-04-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Hydrogen sulfide; Oxidative stress; Voltage-operated calcium channels; Cardiomyoblasts; Calcium signaling
• Online Access: http://www.karger.com/Article/FullText/358690
• ISSN: 1015-8987; 1421-9778

Background: Hydrogen sulfide contributes to the reduction of oxidative stress-related injury in cardiomyocytes but the underlying mechanism is still unclear. Aims: 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 Ni2+ 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.