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 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.
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 H2Sdonor (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: Olan Jackson-Weaver; Jessica M Osmond; Jay S Naik; Laura V Gonzalez Bosc; Benjimen R Walker; Nancy L Kanagy Journal: Am J Physiol Heart Circ Physiol Date: 2015-09-25 Impact factor: 4.733
Authors: Ricardo de Pascual; Andrés M Baraibar; Iago Méndez-López; Martín Pérez-Ciria; Ignacio Polo-Vaquero; Luis Gandía; Sunny E Ohia; Antonio G García; Antonio M G de Diego Journal: Pflugers Arch Date: 2018-05-02 Impact factor: 3.657