Anti-oxidative, anti-cancer and anti-inflammatory actions by thioredoxin 1 and thioredoxin-binding protein-2

Watanabe, Rie; Nakamura, Hajime; Masutani, Hiroshi; Yodoi, Junji

doi:10.1016/j.pharmthera.2010.04.004

Cited by 121 publications

(77 citation statements)

References 122 publications

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“…TXNIP has been identified as a key component linking ROS formation to NLRP3 inflammasome stimulation ; thus it is reasonable to assume that TXNIP inhibition might be useful to downmodulate inflammasome activity. In view of its involvement in lipid/glucose metabolism, various avenues to control TXNIP expression and function have been explored, but attempts to inhibit inflammasome activity by this route are still very preliminary (Watanabe et al, 2010). In alternative to conventional small drug therapeutics, increasing the synthesis of TXNIP-destabilizing miRNA (miRNA-17) might be pursued to downmodulate TXNIP activity (Lerner et al, 2012).…”

Section: Inflammasome Blockers As Novel Therapeuticsmentioning

confidence: 99%

The Therapeutic Potential of Modifying Inflammasomes and NOD-Like Receptors

2013

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Section: Inflammasome Blockers As Novel Therapeuticsmentioning

confidence: 99%

The Therapeutic Potential of Modifying Inflammasomes and NOD-Like Receptors

2013

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“…101 The same study also demonstrated that TXNIP is also commonly overexpressed in AML patients. Considering that TXNIP binds to and inactivates TRX (an important protein in antioxidant defense), 102 the association of TXNIP expression with AML in mice (and in patients) may in part be because of TXNIP-induced oxidative stress. The sources 5820 HOLE et al BLOOD, 2 JUNE 2011 ⅐ VOLUME 117, NUMBER 22…”

Section: Ros Production In Myeloid Diseasementioning

confidence: 99%

Do reactive oxygen species play a role in myeloid leukemias?

Hole

Darley

Tonks

2011

Blood

209

196

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Reactive oxygen species (ROS) are a heterogeneous group of molecules that are generated by mature myeloid cells during innate immune responses, and are also implicated in normal intracellular signaling. Excessive production of ROS (and/or a deficiency in antioxidant pathways) can lead to oxidative stress, a state that has been observed in several hematopoietic malignancies including acute and chronic myeloid leukemias (AML and CML). Currently it is unclear what the cause of oxidative stress might be and whether oxidative stress contributes to the development, progression, or maintenance of these diseases. This article reviews the current evidence suggesting a role for ROS both in normal hematopoiesis and in myeloid leukemogenesis, and discusses the usefulness of therapeutically targeting oxidative stress in myeloid malignancy. (Blood. 2011;117(22):5816-5826) IntroductionOver the past 15 years, there has been a growing appreciation that reactive oxygen species (ROS) production plays an important role in a variety of cellular processes, in addition to their antimicrobial role during phagocytosis by cells of the innate immune system. Specifically, ROS generated by the mitochondria or nicotinamide adenine dinucleotide phosphate (NADPH) oxidases have been shown to influence cell-cycle progression, cell motility, and growth factor signaling in a variety of normal cell types. 1 Many pathologic states are accompanied by excessive cellular ROS production and/or a deficiency in antioxidant defenses, leading to a state known as oxidative stress. 2 Evidence for chronic oxidative stress has been found in many cancers, both in solid tumors such as prostate carcinoma 3 and melanoma 4 and in several hematopoietic malignancies including acute lymphoblastic leukemia (ALL), 5 myelodysplastic syndrome (MDS), 6 and myeloid leukemias including chronic myeloid leukemia (CML) and acute myeloid leukemia (AML). 7 The importance of the association between oxidative stress and malignancy is not currently clear; however, there is evidence that tumor-derived ROS may promote cell survival, 8-10 migration and metastasis, 11,12 proliferation, 13,14 and even drug-resistance, 15 depending on the origin of the cancer. These observations suggest that oxidative stress may subvert the normal roles of ROS so as to benefit the malignant clone.In the context of AML, a recent report indicates that relapse in this disease is associated with increased markers of oxidative stress within the leukemic blasts, suggesting that ROS production may be an important factor in AML progression. 16 Indeed, recent published data from our group suggest that constitutively active Ras (one of the most common abnormalities detected in AML) is capable of driving ROS production in CD34 ϩ human hematopoietic progenitor cells, and this significantly contributes to the mutant Ras phenotype. 17 Furthermore, ROS production appears to contribute to proliferation and migration of hematopoietic cells expressing a variety of oncogenic tyrosine kinases. 18 Thus, increased oxidative s...

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“…These findings may be due to differences between the systemic environment and the local intrafollicular environment. TBP2 was originally identified as a negative regulator of TRX and acts as a suppressor of cell growth and regulator of lipid/glucose metabolism (Watanabe et al 2010). In addition, TBP2 may enhance the atherosclerotic process by increasing vascular inflammation (World et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Alteration in the intrafollicular thiol–redox system in infertile women with endometriosis

Choi¹,

Cho²,

Seo³

et al. 2015

Reproduction

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The aim of this study was to compare intrafollicular biomarkers of thiol-redox system and chronic inflammation in infertile patients with and without endometriosis, and examine correlations between biomarkers and IVF outcomes. The study included 65 patients receiving IVF: 31 patients with endometriosis vs 34 patients without endometriosis. Follicular fluid (FF) was obtained from a single-dominant follicle during oocyte retrieval and stored at K70 8C. Malondialdehyde, superoxide dismutase, glutathione (GSH), glutathione peroxidase 3 (GPX3), thioredoxin (TRX), TRX-binding protein 2 (TBP2), and peroxiredoxin-4 levels were measured in the FF samples by ELISAs as biomarkers of oxidative stress. The inflammatory cytokines interleukin 1 beta (IL1b), IL6, IL8, and tumor-necrosis factor alpha (TNFa) were also measured by ELISAs. GSH levels were significantly lower in the endometriosis group compared with the controls. TBP2 levels were significantly higher in the endometriosis group. IL6, IL8, and TNFa levels were significantly higher in the endometriosis group. The levels of all of the inflammatory cytokines positively correlated with the levels of TRX. GSH levels positively correlated with the number of high-quality embryos. GPX3 and TRX levels negatively correlated with the percentage of mature oocytes. TNFa levels negatively correlated with the cumulative embryo score per embryo. Logistic regression analysis revealed that the number of high-quality embryos was an independent factor predicting clinical pregnancy. In conclusion, there may be an imbalance in the thiol-redox system and increased levels of inflammatory cytokines in the intrafollicular microenvironment of infertile patients with endometriosis, which may affect the qualities of the oocyte and embryo. Reproduction (2015) 149 155-162

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Anti-oxidative, anti-cancer and anti-inflammatory actions by thioredoxin 1 and thioredoxin-binding protein-2

Cited by 121 publications

References 122 publications

The Therapeutic Potential of Modifying Inflammasomes and NOD-Like Receptors

The Therapeutic Potential of Modifying Inflammasomes and NOD-Like Receptors

Do reactive oxygen species play a role in myeloid leukemias?

Alteration in the intrafollicular thiol–redox system in infertile women with endometriosis

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