Altered intracellular redox status in Gaucher disease fibroblasts and impairment of adaptive response against oxidative stress

2007 ◽  
Vol 212 (1) ◽  
pp. 223-235 ◽  
Author(s):  
Marta Deganuto ◽  
Maria Gabriela Pittis ◽  
Alex Pines ◽  
Silvia Dominissini ◽  
Mark R. Kelley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adaptive Response ◽  
Gaucher Disease ◽  
Redox Status ◽  
Intracellular Redox Status ◽  
Intracellular Redox

Canalicular Mrp2 localization is reversibly regulated by the intracellular redox status

2008 ◽  
Vol 295 (5) ◽  
pp. G1035-G1041 ◽  
Author(s):  
Shuichi Sekine ◽  
Kousei Ito ◽  
Toshiharu Horie
Keyword(s):  
Oxidative Stress ◽  
Rat Hepatocytes ◽  
Redox Status ◽  
Intracellular Camp ◽  
Isolated Rat Hepatocytes ◽  
Tertiary Butyl ◽  
Canalicular Membrane ◽  
Internalization Process ◽  
Intracellular Redox Status ◽  
Intracellular Redox

Oxidative stress is known to be a common feature of cholestatic syndrome. We have described the internalization of multidrug resistance-associated protein 2 (Mrp2), a biliary transporter involved in bile salt-independent bile flow, under acute oxidative stress, and a series of signaling pathways finally leading to the activation of novel protein kinase C were involved in this mechanism; however, it has been unclear whether the internalized Mrp2 localization was relocalized to the canalicular membrane when the intracellular redox status was recovered from oxidative stress. In this study, we demonstrated that decreased canalicular expression of Mrp2 induced by tertiary-butyl hydroperoxide (t-BHP) was recovered to the canalicular membrane by the replenishment of GSH by GSH-ethyl ester, a cell-permeable form of GSH. Moreover, pretreatment of isolated rat hepatocytes with colchicine and PKA inhibitor did not affect the t-BHP-induced Mrp2 internalization process but did prevent the Mrp2 recycling process induced by GSH replenishment. Moreover, intracellular cAMP concentration similarly changed with the change of intracellular GSH content. Taken together, our data clearly indicate that the redox-sensitive balance of PKA/PKC activation regulates the reversible Mrp2 localization in two different pathways, the microtubule-independent internalization pathway and -dependent recycling pathway of Mrp2.

scholarly journals A p53-p66Shc signalling pathway controls intracellular redox status, levels of oxidation-damaged DNA and oxidative stress-induced apoptosis

Oncogene ◽  
2002 ◽  
Vol 21 (24) ◽  
pp. 3872-3878 ◽  
Author(s):  
Mirella Trinei ◽  
Marco Giorgio ◽  
Angelo Cicalese ◽  
Sara Barozzi ◽  
Andrea Ventura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox Status ◽  
Signalling Pathway ◽  
Induced Apoptosis ◽  
And Oxidative Stress ◽  
Intracellular Redox Status ◽  
Intracellular Redox ◽  
Damaged Dna

scholarly journals The Onset of Tacrolimus Biosynthesis in Streptomyces tsukubaensis Is Dependent on the Intracellular Redox Status

Antibiotics ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 703
Author(s):  
Sílvia D. S. Pires ◽  
Rute Oliveira ◽  
Pedro Moradas-Ferreira ◽  
Marta V. Mendes
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Metabolic Flux ◽  
Redox Status ◽  
Oxidative Stress Response ◽  
Molecular Response ◽  
Streptomyces Tsukubaensis ◽  
The Impact ◽  
Intracellular Redox Status ◽  
Intracellular Redox

The oxidative stress response is a key mechanism that microorganisms have to adapt to changeling environmental conditions. Adaptation is achieved by a fine-tuned molecular response that extends its influence to primary and secondary metabolism. In the past, the role of the intracellular redox status in the biosynthesis of tacrolimus in Streptomyces tsukubaensis has been briefly acknowledged. Here, we investigate the impact of the oxidative stress response on tacrolimus biosynthesis in S. tsukubaensis. Physiological characterization of S. tsukubaensis showed that the onset of tacrolimus biosynthesis coincided with the induction of catalase activity. In addition, tacrolimus displays antioxidant properties and thus a controlled redox environment would be beneficial for its biosynthesis. In addition, S. tsukubaensis ∆ahpC strain, a strain defective in the H2O2-scavenging enzyme AhpC, showed increased production of tacrolimus. Proteomic and transcriptomic studies revealed that the tacrolimus over-production phenotype was correlated with a metabolic rewiring leading to increased availability of tacrolimus biosynthetic precursors. Altogether, our results suggest that the carbon source, mainly used for cell growth, can trigger the production of tacrolimus by modulating the oxidative metabolism to favour a low oxidizing intracellular environment and redirecting the metabolic flux towards the increase availability of biosynthetic precursors.

scholarly journals Regulation of CD20 expression by radiation-induced changes in intracellular redox status

2008 ◽  
Vol 44 (4) ◽  
pp. 614-623 ◽  
Author(s):  
Damodar Gupta ◽  
Meredith E. Crosby ◽  
Alexandru Almasan ◽  
Roger M. Macklis
Keyword(s):  
Redox Status ◽  
Cd20 Expression ◽  
Radiation Induced ◽  
Induced Changes ◽  
Intracellular Redox Status ◽  
Intracellular Redox

Redox-based regulation of neural stem cell function and Nrf2

2015 ◽  
Vol 43 (4) ◽  
pp. 627-631 ◽  
Author(s):  
Lalitha Madhavan
Keyword(s):  
Oxidative Stress ◽  
Stress Resistance ◽  
Somatic Mutations ◽  
Cell Function ◽  
Therapeutic Potential ◽  
Redox Status ◽  
Common Theme ◽  
Tissue Microenvironment ◽  
Neural Tissues ◽  
Intracellular Redox Status

Neural stem cells (NSCs) play vital roles in the development and maintenance of brain tissues throughout life. They can also potentially act as powerful sources of regeneration and repair during pathology to replace degenerating cells and counteract deleterious changes in the tissue microenvironment. However, both aging and neurodegeneration involve an up-regulation of processes, such as oxidative stress, inflammation, somatic mutations, and reduction in growth factors in neural tissues, which threaten the robust functioning of NSCs. Nevertheless, recent evidence also indicates that NSCs may possess the intrinsic capability to cope with such stressors in their microenvironment. Whereas the mechanisms governing the responses of NSCs to stress are diverse, a common theme that is emerging suggests that underlying changes in intracellular redox status are crucial. Here we discuss such redox-based regulation of NSCs, particularly in relation to nuclear erythroid factor 2-like 2 (Nrf2), which is a key cellular stress resistance factor, and its implications for successfully harnessing NSC therapeutic potential towards developing cell-based therapeutics for nervous system disorders.

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