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1.
Journal of Zhejiang University. Science. B ; (12): 310-321, 2019.
Artigo em Inglês | WPRIM | ID: wpr-1010462

RESUMO

OBJECTIVE@#Reactive oxygen species (ROS) are involved in a variety of biological phenomena and serve both deleterious and beneficial roles. ROS quantification and assessment of reaction networks are desirable but difficult because of their short half-life and high reactivity. Here, we describe a pro-oxidative model in a single human lung carcinoma SPC-A-1 cell that was created by application of extracellular H2O2 stimuli.@*METHODS@#Modified microfluidics and imaging techniques were used to determine O2 •- levels and construct an O2 •- reaction network. To elucidate the consequences of increased O2 •- input, the mitochondria were given a central role in the oxidative stress mode, by manipulating mitochondria-interrelated cytosolic Ca2+ levels, mitochondrial Ca2+ uptake, auto-amplification of intracellular ROS and the intrinsic apoptotic pathway.@*RESULTS AND CONCLUSIONS@#Results from a modified microchip demonstrated that 1 mmol/L H2O2 induced a rapid increase in cellular O2 •- levels (>27 vs. >406 amol in 20 min), leading to increased cellular oxidizing power (evaluated by ROS levels) and decreased reducing power (evaluated by glutathione (GSH) levels). In addition, we examined the dynamics of cytosolic Ca2+ and mitochondrial Ca2+ by confocal laser scanning microscopy and confirmed that Ca2+ stores in the endoplasmic reticulum were the primary source of H2O2-induced cytosolic Ca2+ bursts. It is clear that mitochondria have pivotal roles in determining how exogenous oxidative stress affects cell fate. The stress response involves the transfer of Ca2+ signals between organelles, ROS auto-amplification, mitochondrial dysfunction, and a caspase-dependent apoptotic pathway.


Assuntos
Humanos , Apoptose , Cálcio/metabolismo , Sinalização do Cálcio , Caspases/metabolismo , Linhagem Celular Tumoral , Linhagem da Célula , Citosol/metabolismo , Glutationa/metabolismo , Peróxido de Hidrogênio/química , Mitocôndrias/metabolismo , Oxirredução , Estresse Oxidativo , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais , Superóxidos/química
2.
Acta Physiologica Sinica ; (6): 186-192, 2015.
Artigo em Chinês | WPRIM | ID: wpr-255958

RESUMO

This study was aimed to investigate the mechanism of all-trans retinoic acid (ATRA) up-regulating apelin expression in vascular smooth muscle cells (VSMCs). The effect of ATRA on apelin expression in the VSMCs was investigated by RT-PCR, real-time PCR and Western blot analysis. To further define whether retinoic acid receptor α (RARα) mediated the induction of apelin by ATRA, endogenous RARα was down regulated by transfection of siRNA against RARα (si-RARα) or RARα was over-expressed by infection of the adenovirus vector pAd-GFP-RARα in the VSMCs. The results showed that ATRA significantly induced apelin expression in a time- and dose-dependent manner in the VSMCs. Although RARα expression was increased in a time-dependent manner, the expressions of RARβ and RARγ were little changed by the ATRA treatment. When VSMCs were treated with a RARα antagonist Ro 41-5253 prior to the addition of ATRA, or si-RARα was used to down regulate endogenous RARα expression, the blockade of RARα signaling partially reduced the response of apelin to ATRA. Moreover, RARα over-expression, induced by infection of pAd-GFP-RARα, further increased the induction of apelin by ATRA. In conclusion, ATRA may up-regulate apelin expression in VSMCs, and the mechanism may be RARα dependent.


Assuntos
Benzoatos , Cromanos , Regulação da Expressão Gênica , Peptídeos e Proteínas de Sinalização Intercelular , Metabolismo , Músculo Liso Vascular , Biologia Celular , Miócitos de Músculo Liso , Metabolismo , Reação em Cadeia da Polimerase em Tempo Real , Receptores do Ácido Retinoico , Metabolismo , Receptor alfa de Ácido Retinoico , Transdução de Sinais , Transfecção , Tretinoína , Metabolismo , Regulação para Cima
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