ArticleFree radical biology & medicine2015
Adenovirus-mediated transfer of the SOCS-1 gene to mouse lung confers protection against hyperoxic acute lung injury.
Article in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Advances in research on hyperoxia-induced acute lung injury: from pathogenesis to therapy.Frontiers in cell and developmental biology · 2026Review
- Oxidative stress in ARDS: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- LncRNAMolecules (Basel, Switzerland) · 2022Article
- Lung fibrosis is induced in ADAR2 overexpressing mice via HuR-induced CTGF signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- MicroRNA-23a-5p Is Involved in the Regulation of Lipopolysaccharide-Induced Acute Lung Injury by Targeting HSP20/ASK1.Oxidative medicine and cellular longevity · 2021Article
- MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1.Molecules (Basel, Switzerland) · 2020Article
- Alda-1 Attenuates Hyperoxia-Induced Acute Lung Injury in Mice.Frontiers in pharmacology · 2020Article
- SOCS-1 Suppresses Inflammation Through Inhibition of NALP3 Inflammasome Formation in Smoke Inhalation-Induced Acute Lung Injury.Inflammation · 2018Article
- Akap1 genetic deletion increases the severity of hyperoxia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Differential responses of innate immunity triggered by different subtypes of influenza a viruses in human and avian hosts.BMC medical genomics · 2017Article
- SOCS-1 rescues IL-1β-mediated suppression of epithelial sodium channel in mouse lung epithelial cells via ASK-1.Oncotarget · 2016Article
- Deletion of P2X7 attenuates hyperoxia-induced acute lung injury via inflammasome suppression.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis.Mediators of inflammation · 2016Article
- Article
- miRNA-101 inhibits ovarian cancer cells proliferation and invasion by down-regulating expression of SOCS-2.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Suppressor of cytokine signaling-1 (SOCS-1) is a member of the suppressor of cytokine signaling family of proteins and an inhibitor of interleukin-6 (IL-6) signaling. SOCS-1 has been shown to protect cells from cellular damage and apoptosis induced by tumor necrosis factor (TNF), lipopolysaccharide (LPS), and interferon gamma (IL-γ). However, it is not known whether increased SOCS-1 is protective during pulmonary oxidative stress. Therefore, we hypothesized that increased SOCS-1 in the lungs of mice would be protective in the setting of hyperoxic lung injury. We administered SOCS-1 adenovirus (Ad-SOCS-1) intratracheally into the lungs and exposed the mice to 100% O2. Mice infected with GFP adenovirus (Ad-GFP) were used as controls. Mice treated with Ad-SOCS-1 had enhanced survival in 100% oxygen compared to Ad-GFP-administered mice. After 3 days of hyperoxia, Ad-GFP mice were ill and tachypnic and died after 4 days. In contrast, all Ad-SOCS-1-treated mice survived for at least 6 days in hyperoxia and 80% survived beyond 7 days. Ad-SOCS-1 transfection protected mouse lungs from injury as indicated by lower lung wet/dry weight, alveolar-capillary protein leakage, reduced infiltration of inflammatory cells, and lower content of thiobarbituric acid-reactive substances in lung homogenate. Our results also indicated that Ad-SOCS-1 significantly inhibits hyperoxia-induced ASK-1 (apoptosis signal-regulating kinase 1) expression. Taken together, these findings show that increased expression of adenovirus-mediated SOCS-1 in the lungs of mice significantly protects against hyperoxic lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.