Extracellular Superoxide Dismutase in Pulmonary Fibrosis

Gao, Fei; Kinnula, Vuokko L.; Myllärniemi, Marjukka; Oury, Tim D.

doi:10.1089/ars.2007.1908

Cited by 109 publications

(81 citation statements)

References 136 publications

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“…Moreover, the antioxidant response observed in several studies depended on the cell type in which it was determined. For example, some studies showed a genomic response through ROS-nrf2 pathways in cells with nuclei such as lung tissue, a factor that produces a diff erence with our study (Gao et al, 2008;Edeas et al, 2009). In our study, we use erythrocyte lysate, wherein the activity may refl ect transient changes that may not be statistically signifi cant.…”

Section: Discussionsupporting

confidence: 41%

Relationship between severity of adult community-acquired pneumonia and impairment of the antioxidant defense system

Castillo

Carrasco

Álvarez³

et al. 2013

Biol. Res.

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Oxidant/antioxidant imbalance has been reported in some infectious diseases, including community-acquired pneumonia (CAP). The aim was to assess the antioxidant status in adults with CAP and its relationship with clinical severity at admission. Fifty-nine patients with CAP were enrolled and categorized at admission by the FINE score, from July 2010 to October 2012. In the same period 61 controls were enrolled. Plasma samples were obtained at admission for determination of the ferric reducing ability of plasma (FRAP) and lipid peroxidation (8-isoprostane). Erythrocyte reduced (GSH)/oxidized (GSSG) glutathione, malondialdehyde (MDA) and antioxidant enzyme activity were assessed. Antioxidant status in adults with CAP represented by FRAP and the GSH/GSSG ratio were 16.8% (p=0.03) and 39.7% (p=0.04) lower than control values, respectively. In addition, FRAP values showed a positive correlation with GSH/GSSG ratio (r=0.852; p<0.02; n=59). The CAP group showed greater lipid peroxidation in both plasma and erythrocytes. The FINE score correlated negatively with FRAP (r= -0.718; p<0.05; n=59) and positively with MDA and F2 isoprostane levels (r=0.673; p<0.05; n=59; r=0.892; p<0.01; n=59, respectively). Antioxidant status alterations correlated with clinical severity. The FRAP assay and lipid peroxidation biomarkers may provide a useful parameter for estimating the severity and the clinical outcome of patients with CAP.

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Section: Discussionsupporting

confidence: 41%

Relationship between severity of adult community-acquired pneumonia and impairment of the antioxidant defense system

Castillo

Carrasco

Álvarez³

et al. 2013

Biol. Res.

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“…31 Specific SOD3 polymorphisms have also been associated with varying courses of idiopathic pulmonary fibrosis in humans, further supporting the role of this protein in protecting against lung disease. 32 We propose that loss of SOD3 might underlie the progression of lung disease observed following diverse stimuli that would impose an initial oxidant stress, such as infection, radiation, hemorrhage, or trauma.…”

Section: Discussionmentioning

confidence: 99%

Loss of Extracellular Superoxide Dismutase Leads to Acute Lung Damage in the Presence of Ambient Air

Góngora

Lob

Landmesser

et al. 2008

The American Journal of Pathology

113

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The extracellular superoxide dismutase 3 (SOD3) is highly expressed in both blood vessels and lungs. In different models of pulmonary injury, SOD3 is reduced; however, it is unclear whether this contributes to lung injury. To study the role of acute SOD3 reduction in lung injury, the SOD3 gene was deleted in adult mice by using the Cre-Lox technology. Acute reduction of SOD3 led to a fivefold increase in lung superoxide, marked inflammatory cell infiltration, a threefold increase in the arterial-alveolar gradient, respiratory acidosis, histological changes similar to those observed in adult respiratory distress syndrome, and 85% mortality. Treatment with the SOD mimetic MnTBAP and intranasal administration of SOD-containing polyketal microparticles reduced mortality, prevented the histological alterations, and reduced lung superoxide levels. To understand how mice with the SOD3 embryonic deletion survived without lung injury, gene array analysis was performed. These data demonstrated the up-regulation of 37 genes and down-regulation of nine genes, including those involved in cell signaling, inflammation, and gene transcription in SOD3 ؊/؊ mice compared with either mice with acute SOD3 reduction or wildtype controls. These studies show that SOD3 is essential for survival in the presence of ambient oxygen and that acute loss of this enzyme can lead to severe

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“…Furthermore, adoptive transfer of MSC also efficiently counteracted infiltration of immune cells at early (44) and at late stages as shown here. This is particularly important since oxidative stress generated by radiotherapy or chemotherapy is known to initiate a cascade of acute and chronic inflammatory reactions that may further increase oxidative stress in the inflamed tissue (3,30). Thus, by addressing both, oxidative stress and tissue inflammation, MSC therapy may serve as an ideal mitigator of adverse late effects of radiotherapy.…”

Section: Murine Wt Bm (Xrt/bm) Cells From C57bl/6 Donor Mice Into Thementioning

confidence: 99%

Mesenchymal Stem Cell Therapy Protects Lungs from Radiation-Induced Endothelial Cell Loss by Restoring Superoxide Dismutase 1 Expression

Klein

Steens

Wiesemann

et al. 2017

Antioxidants & Redox Signaling

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Aims: Radiation-induced normal tissue toxicity is closely linked to endothelial cell (EC) damage and dysfunction (acute effects). However, the underlying mechanisms of radiation-induced adverse late effects with respect to the vascular compartment remain elusive, and no causative radioprotective treatment is available to date. Results: The importance of injury to EC for radiation-induced late toxicity in lungs after whole thorax irradiation (WTI) was investigated using a mouse model of radiation-induced pneumopathy. We show that WTI induces EC loss as long-term complication, which is accompanied by the development of fibrosis. Adoptive transfer of mesenchymal stem cells (MSCs) either derived from bone marrow or aorta (vascular wall-resident MSCs) in the early phase after irradiation limited the radiation-induced EC loss and fibrosis progression. Furthermore, MSC-derived culture supernatants rescued the radiation-induced reduction in viability and longterm survival of cultured lung EC. We further identified the antioxidant enzyme superoxide dismutase 1 (SOD1) as a MSC-secreted factor. Importantly, MSC treatment restored the radiation-induced reduction of SOD1 levels after WTI. A similar protective effect was achieved by using the SOD-mimetic EUK134, suggesting that MSCderived SOD1 is involved in the protective action of MSC, presumably through paracrine signaling. Innovation: In this study, we explored the therapeutic potential of MSC therapy to prevent radiation-induced EC loss (late effect) and identified the protective mechanisms of MSC action. Conclusions: Adoptive transfer of MSCs early after irradiation counteracts radiation-induced vascular damage and EC loss as late adverse effects. The high activity of vascular wall-derived MSCs for radioprotection may be due to their tissue-specific action. Antioxid. Redox Signal. 26, 563-582.

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Extracellular Superoxide Dismutase in Pulmonary Fibrosis

Cited by 109 publications

References 136 publications

Relationship between severity of adult community-acquired pneumonia and impairment of the antioxidant defense system

Relationship between severity of adult community-acquired pneumonia and impairment of the antioxidant defense system

Loss of Extracellular Superoxide Dismutase Leads to Acute Lung Damage in the Presence of Ambient Air

Mesenchymal Stem Cell Therapy Protects Lungs from Radiation-Induced Endothelial Cell Loss by Restoring Superoxide Dismutase 1 Expression

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