Lopez-Pedrera, C. (Chary)

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1996 - 199912000 - 20102

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    Pharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cells
    (International Institute of Anticancer Research, 2010) Rodriguez-Ariza, A. (Antonio); Corrales, F.J. (Fernando José); Lopez-Pedrera, C. (Chary); Lopez-Sanchez, L.M. (Laura M.); Aranda, E. (E.)
    BACKGROUND/AIM: S-Nitrosoglutathione reductase (GSNOR) and thioredoxin enzyme systems participate in cellular defence against nitrosative stress. Pharmacological interventions against these enzyme systems might represent valuable strategies to impair S-nitrosothiol (SNO) homeostasis in tumour cells. MATERIALS AND METHODS: Human HepG2 cells were pre-treated with mithramycin A or auranofin and exposed to S-nitroso-L-cysteine. GSNOR mRNA levels were analyzed by quantitative real-time reverse transcriptase-polymerase chain reaction and S-nitrosated proteins were detected and purified using the biotin-switch approach. Proteins were identified using electrospray ionization tandem mass spectrometry. RESULTS: Mithramycin interfered with GSNOR induction resulting in an increased cellular sensitivity to protein S-nitrosation. Moreover, the thioredoxin reductase inhibitor auranofin also increased cellular susceptibility to S-nitrosoprotein formation. The impairment of these two cellular defense systems against nitrosative stress resulted in different sets of S-nitrosated proteins, as revealed by the proteomics approach. CONCLUSION: Our results suggest that pharmacological intervention with mithramycin or auranofin may constitute promising tools for altering SNO homeostasis in tumour cells.
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    Patogénesis y tratamiento de la alteración hemostática en la leucemia aguda promielocítica
    (Elsevier, 1996) Paramo, J.A. (José Antonio); Lopez-Pedrera, C. (Chary); Velasco, F. (Francisco)
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    Regulation by nitric oxide of endotoxin-induced tissue factor and plasminogen activator inhibitor-1 in endothelial cells
    (Schattauer, 2002) Paramo, J.A. (José Antonio); Lopez-Pedrera, C. (Chary); Rocha, E. (Eduardo); Hermida, J. (José); Orbe, J. (Josune); Perez-Ruiz, A. (Ana); Velasco, F. (Francisco); Montes, R. (Ramón)
    The increase in nitric oxide (NO) production in lipopolysaccharide (LPS)-induced sepsis is thought to contribute to the development of shock. However, NO could also play an antithrombotic role. Little is known about the modulating effect of NO on the endothelial overexpression and production of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) occurring in endotoxemia. We analyzed the effect of N(G)-nitro-L-arginine-methyl-ester (L-NAME), an inhibitor of NO synthases, and S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, on the expression and synthesis of TF and PAI-1 by LPS-challenged human umbilical vein endothelial cells (HUVEC): L-NAME enhanced the increase in TF mRNA and antigen levels (P <0.05) observed in LPS-treated HUVEC; SNAP down-regulated the LPS-induced TF increment (p <0.05). However, no effects of NO on regulation of the LPS-dependent increase in PAI-1 could be seen. Thus, NO could play an antithrombotic role in sepsis by down-regulating the endothelial overexpression and production of TF.