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. © 2014 S. Karger AG, Basel.

ROLE OF CALCIUM CHANNELS IN THE PROTECTIVE EFFECT OF HYDROGEN SULFIDE IN RAT CARDIOMYOBLASTS

AVANZATO, DANIELE;MERLINO, ANNALISA;MUNARON, Luca Maria;MANCARDI, Daniele
2014

Abstract

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. © 2014 S. Karger AG, Basel.
33
4
1205
1214
Daniele Avanzato; Annalisa Merlino; Sabina Porrera; Rui Wang; Luca Munaron; Daniele Mancardi
File in questo prodotto:
File Dimensione Formato  
avanzato et al.pdf

Accesso aperto

Tipo di file: PDF EDITORIALE
Dimensione 1.34 MB
Formato Adobe PDF
1.34 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/144661
Citazioni
  • ???jsp.display-item.citation.pmc??? 11
  • Scopus 31
  • ???jsp.display-item.citation.isi??? 28
social impact