Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases

Nguyen, Nguyen Hoai; Tran, Gia-Buu; Nguyen, Cattien V.

doi:10.1007/s00109-019-01845-2

Cited by 90 publications

(71 citation statements)

References 79 publications

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“…Along with anti-tumor activity, SOD3 also exhibit anti-autoimmune potential. Overexpression of SOD3 found to ameliorate several auto-immune diseases such as arthritis, psoriasis (48) and the alternation in the level of SOD3 found to be associated in inflammatory bowel diseases and systemic lupus erythematosus (49,50). These studies emphasized the importance of SOD3 as an anti-tumor and anti-autoimmune bio-compound.…”

Section: Discussionmentioning

confidence: 94%

Superoxide Dismutase 3 Controls the Activation and Differentiation of CD4+T Cells

et al. 2021

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Superoxide dismutase 3 (SOD3), a well-known antioxidant has been shown to possess immunomodulatory properties through inhibition of T cell differentiation. However, the underlying inhibitory mechanism of SOD3 on T cell differentiation is not well understood. In this study, we investigated the effect of SOD3 on anti-CD3/CD28- or phorbol myristate acetate (PMA) and ionomycin (ION)-mediated activation of mouse naive CD4+ T cells. Our data showed that SOD3 suppressed the expression of activation-induced surface receptor proteins such as CD25, and CD69, and cytokines production. Similarly, SOD3 was found to reduce CD4+T cells proliferation and suppress the activation of downstream pathways such as ERK, p38, and NF-κB. Moreover, naïve CD4+T cells isolated from global SOD3 knock-out mice showed higher expression of CD25, CD69, and CD71, IL-2 production, proliferation, and downstream signals compared to wild-type CD4+T cells. Whereas, the use of DETCA, a known inhibitor of SOD3 activity, found to nullify the inhibitory effect of SOD3 on CD4+T cell activation of both SOD3 KO and wild-type mice. Furthermore, the expression of surface receptor proteins, IL-2 production, and downstream signals were also reduced in Th2 and Th17 differentiated cells upon SOD3 treatment. Overall, our data showed that SOD3 can attenuate CD4+T cell activation through modulation of the downstream signalings and restrict CD4+T cell differentiation. Therefore, SOD3 can be a promising therapeutic for T cell-mediated disorders.

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Section: Discussionmentioning

confidence: 94%

Superoxide Dismutase 3 Controls the Activation and Differentiation of CD4+T Cells

et al. 2021

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“…Superoxide dismutases (SODs), categorized as cytosolic SOD1, mitochondrial SOD2, and extracellular SOD3, are widely distributed in various cellular compartments and can rapidly dismutate superoxide into H 2 O 2 73 . Then, peroxiredoxin (PRX), glutathione peroxidase (GPX) and catalase (CAT) convert H 2 O 2 into water (H 2 O).…”

Section: Antioxidant Defense Mechanismsmentioning

confidence: 99%

The double-edged roles of ROS in cancer prevention and therapy

et al. 2021

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Reactive oxygen species (ROS) serve as cell signaling molecules generated in oxidative metabolism and are associated with a number of human diseases. The reprogramming of redox metabolism induces abnormal accumulation of ROS in cancer cells. It has been widely accepted that ROS play opposite roles in tumor growth, metastasis and apoptosis according to their different distributions, concentrations and durations in specific subcellular structures. These double-edged roles in cancer progression include the ROS-dependent malignant transformation and the oxidative stress-induced cell death. In this review, we summarize the notable literatures on ROS generation and scavenging, and discuss the related signal transduction networks and corresponding anticancer therapies. There is no doubt that an improved understanding of the sophisticated mechanism of redox biology is imperative to conquer cancer.

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“…The vast majority of H 2 O 2 arises from intracellular sources, i.e., mitochondrial superoxide dismutase (SOD2) [78], peroxisome molecular machinery (organelle associated with lipid metabolism, [79,80]), and cytoplasmic superoxide dismutase 1 (SOD1) [81]. The main extracellular source of H 2 O 2 is derived from the activity of superoxide dismutase 3 (SOD3) [82].…”

Section: Iron Oxide and Redox Homeostasismentioning

confidence: 99%

The Intrinsic Biological Identities of Iron Oxide Nanoparticles and Their Coatings: Unexplored Territory for Combinatorial Therapies

2020

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Over the last 20 years, iron oxide nanoparticles (IONPs) have been the subject of increasing investigation due to their potential use as theranostic agents. Their unique physical properties (physical identity), ample possibilities for surface modifications (synthetic identity), and the complex dynamics of their interaction with biological systems (biological identity) make IONPs a unique and fruitful resource for developing magnetic field-based therapeutic and diagnostic approaches to the treatment of diseases such as cancer. Like all nanomaterials, IONPs also interact with different cell types in vivo, a characteristic that ultimately determines their activity over the short and long term. Cells of the mononuclear phagocytic system (macrophages), dendritic cells (DCs), and endothelial cells (ECs) are engaged in the bulk of IONP encounters in the organism, and also determine IONP biodistribution. Therefore, the biological effects that IONPs trigger in these cells (biological identity) are of utmost importance to better understand and refine the efficacy of IONP-based theranostics. In the present review, which is focused on anti-cancer therapy, we discuss recent findings on the biological identities of IONPs, particularly as concerns their interactions with myeloid, endothelial, and tumor cells. Furthermore, we thoroughly discuss current understandings of the basic molecular mechanisms and complex interactions that govern IONP biological identity, and how these traits could be used as a stepping stone for future research.

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Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases

Cited by 90 publications

References 79 publications

Superoxide Dismutase 3 Controls the Activation and Differentiation of CD4+T Cells

Superoxide Dismutase 3 Controls the Activation and Differentiation of CD4+T Cells

The double-edged roles of ROS in cancer prevention and therapy

The Intrinsic Biological Identities of Iron Oxide Nanoparticles and Their Coatings: Unexplored Territory for Combinatorial Therapies

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