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Neutrophils restrain sepsis associated coagulopathy via extracellular vesicles carrying superoxide dismutase 2 in a murine model of lipopolysaccharide induced sepsis

ABSTRACT: Neutrophils restrain sepsis associated coagulopathy via extracellular vesicles carrying superoxide dismutase 2 in a murine model of lipopolysaccharide induced sepsis

PROVIDER: PRJNA852256 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19805708_1.fastq.gz	Fastqsanger.gz
	SRR19805708_2.fastq.gz	Fastqsanger.gz
	SRR19805709_1.fastq.gz	Fastqsanger.gz
	SRR19805709_2.fastq.gz	Fastqsanger.gz
	SRR19805710_1.fastq.gz	Fastqsanger.gz

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Neutrophils restrain sepsis associated coagulopathy via extracellular vesicles carrying superoxide dismutase 2 in a murine model of lipopolysaccharide induced sepsis

Project description:Disseminated intravascular coagulation (DIC) is a deadly complication of sepsis lacking effective managements. Although excessive inflammatory responses are emerging as key triggers of coagulopathy in sepsis, the interplays between immune system and coagulation are not fully understood. In a murine model of sepsis induced by intraperitoneal lipopolysaccharide (LPS), we found neutrophils in circulation mitigate the occurrence of DIC, thereby preventing the subsequent septic death. We found circulating neutrophils constantly release extracellular vesicles (EVs) containing mitochondria, which carry substantial amount of Superoxide Dismutase 2 (Sod2) upon LPS exposure. The extracellular Sod2 is necessary to bring about neutrophils’ antithrombotic function by eliminating endothelial reactive oxygen species (ROS) accumulation and alleviating endothelial dysfunction. Intervening endothelial ROS accumulation by antioxidants significantly ameliorates DIC with correspondingly improved survival in sepsis. These findings revealed a novel interaction between neutrophils and vascular endothelium which critically regulates coagulation in sepsis and had potential implications for the management of septic DIC.

2022-07-26 | GSE206825 | GEO

Fruit derived superoxide dismutase nanozyme for sepsis-induced acute lung injury therapy

Project description:Fruit derived superoxide dismutase nanozyme for sepsis-induced acute lung injury therapy

| PRJNA1173153 | ENA

Natural plant-derived superoxide dismutase nanoenzyme for sepsis-induced liver injury therapy.

Project description:Natural plant-derived superoxide dismutase nanoenzyme for sepsis-induced liver injury therapy.

| PRJNA1169014 | ENA

Natural plant-derived superoxide dismutase nanoenzyme for sepsis-induced liver injury therapy.

Project description:Sepsis-induced liver injury is an important cause of septicemia deaths, this injury is characterized by an overproduction of reactive oxygen species (ROS) within the liver, which activates the inflammatory response and results in the release of numerous inflammatory factors, ultimately leading to liver damage. Thus, the development of medicines capable of eliminating ROS and reducing inflammatory factors holds significant prospects. In this study, we synthesized and characterized a natural superoxide dismutase-mimicking carbon dots (G-CDs) form a greenery Glycyrrhiza with distinctive ROS scavenging ability for SILI therapy. The abundant surface unsaturated groups especially oxhydry and carbonyl groups enable G-CDs to exhibit excellent SOD-like enzyme activity exceeding 10000 U/mg and significantly reduce the excessive production of ROS and inflammatory factors. In addition, G-CDs reduced inflammation, oxidative damage, and tissue damage in the liver of lipopolysaccharide (LPS) induced SILI mice model. Mechanistically, G-CDs protect liver tissue by activating Keap-1/Nrf-2 mediated antioxidant signaling and inhibiting NF-κB-dependent inflammatory responses. In conclusion, this study establishes the potential of G-CDs as a promising therapeutic agent for the treatment SILI.

2025-09-11 | GSE278841 | GEO

Fruit derived superoxide dismutase nanozyme for sepsis-induced acute lung injury therapy

Project description:As a life-threatening infectious disease in clinics, sepsis is characterized by uncontrolled systemic inflammatory response and multi-organ damage due to the excessive production of reactive oxygen species (ROS). The lung is the most frequently affected organ that is susceptible to developing acute lung injury (ALI) with high morbidity and mortality rates. Nevertheless, there are currently no effective drugs for the treatment of ALI. Herein, we developed a natural superoxide dismutase-mimicking carbon dots (H-CDs) derived from a fruit, hawthorn, with distinctive ROS scavenging ability for ALI therapy. The carboxyl/oxygen-based groups give the generated H-CDs excellent SOD-like activity of > 9000 U mg-1 and acted as a SOD-like nanozyme in the protection of cells from oxidative damage by scavenging ROS and ameliorating the levels of pro-inflammatory factors. Importantly, H-CDs reduced lung inflammatory response, oxidative damage, and histological severity in a lipopolysaccharide (LPS)-induced ALI mice model with minimal adverse effects. Mechanistically, H-CDs protected lung tissues by activating Nrf-2/HO-1 mediated antioxidant signaling and inhibiting NF-κB-dependent inflammatory responses. Collectively, this study establishes the potential of H-CDs as a promising therapeutic agent for the treatment of ALI.

2025-10-27 | GSE279500 | GEO

Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

Project description:Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

| PRJNA664402 | ENA

Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

Project description:Superoxide radical anion and other Reactive Oxygen Species are constantly produced during respiration. In mitochondria, the dismutation of the superoxide radical anion is accelerated by the mitochondrial superoxide dismutase 2 (SOD2), an enzyme that has been traditionally associated with antioxidant protection. However, increases in SOD2 expression promote oxidative stress, indicating that there may be a prooxidant role for SOD2. We show that SOD2, which normally binds manganese, can incorporate iron and generate an alternative isoform with peroxidase activity. The switch from manganese to iron allows FeSOD2 to utilize H2O2 to promote oxidative stress. We found that FeSOD2 is formed in cultured cells. FeSOD2 causes mitochondrial dysfunction and higher levels of oxidative stress in cultured cells. We show that formation of FeSOD2 converts an antioxidant defense into a prooxidant peroxidase that leads to cellular changes seen in multiple human diseases.

2017-12-05 | GSE106206 | GEO

Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

Project description:Compelling evidence support an involvement of oxidative stress and intestinal inflammation as early events in the predisposition and development of obesity and its related comorbidities. Here we show that deficiency of the major mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) in the gastrointestinal tract drives spontaneous obesity. Intestinal epithelium-specific Sod2 ablation in mice induced adiposity, inflammation and insulin resistance via phospholipase A2 (PLA2) activation and increased synthesis of omega-6 polyunsaturated fatty acid arachidonic acid. Remarkably, this obese and hyperinsulinemic phenotype was rescued when fed an essential fatty acid deficient diet, which abrogates de novo biosynthesis of arachidonic acid. Data from clinical samples revealed that the negative correlation between intestinal SOD2 mRNA levels and obesity features, such as body mass index and omega-6/omega-3 fatty acid ratio, appears to be conserved between mice and humans. Collectively, our findings suggest a role of intestinal SOD2 levels, PLA2 activity and arachidonic acid in obesity presenting new potential targets of therapeutic interest in the context of this metabolic disorder.

2021-12-31 | GSE158237 | GEO

Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

Project description:Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

| PRJNA415919 | ENA

Molecular mechanisms of lifespan extension in long-lived mitocondrial superoxide dismutase sod-2 mutants

Project description:Molecular mechanisms of lifespan extension in long-lived mitocondrial superoxide dismutase sod-2 mutants

| PRJNA1208437 | ENA