ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Myeloid depletion of SOCS3 enhances LPS-induced acute lung injury through CCAAT/enhancer binding protein δ pathway.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Network-Based Integrated Analysis of Transcriptomic Studies in Dissecting Gene Signatures for LPS-Induced Acute Lung Injury.Inflammation · 2021Pooled it
- Socs3b regulates the development and function of innate immune cells in zebrafish.Frontiers in immunology · 2023Article
- CEBPD modulates the airway smooth muscle transcriptomic response to glucocorticoids.Respiratory research · 2022Article
- CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.Research (Washington, D.C.) · 2022Review
- Qinbaohong Zhike Oral Liquid Attenuates LPS-Induced Acute Lung Injury in Immature Rats by Inhibiting OLFM4.Oxidative medicine and cellular longevity · 2022Article
- Article
- A Novel Selective Sphingosine Kinase 2 Inhibitor, HWG-35D, Ameliorates the Severity of Imiquimod-Induced Psoriasis Model by Blocking Th17 Differentiation of Naïve CD4 T Lymphocytes.International journal of molecular sciences · 2020Article
- The Complex Relationship between Diabetic Retinopathy and High-Mobility Group Box: A Review of Molecular Pathways and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2020Review
- Resveratrol decreases CD45Journal of cellular and molecular medicine · 2019Article
- Aquaporin 4 Blockade Attenuates Acute Lung Injury Through Inhibition of Th17 Cell Proliferation in Mice.Inflammation · 2019Article
- The Functional Mechanisms of miR-30b-5p in Acute Lung Injury in Children.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Article
- The neutrophil chemoattractant peptide proline-glycine-proline is associated with acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Lack of SOCS3 increases LPS-induced murine acute lung injury through modulation of Ly6C(+) macrophages.Respiratory research · 2017Article
- Article
- Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway.Molecular medicine reports · 2017Article
- S100A8/A9 and S100A9 reduce acute lung injury.Immunology and cell biology · 2017Article
- Platelet-activating Factor Mediates Endotoxin Tolerance by Regulating Indoleamine 2,3-Dioxygenase-dependent Expression of the Suppressor of Cytokine Signaling 3.The Journal of biological chemistry · 2017Article
- Protective effect of suppressing STAT3 activity in LPS-induced acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- SOCS3 revisited: a broad regulator of disease, now ready for therapeutic use?Cellular and molecular life sciences : CMLS · 2016Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Although uncontrolled inflammatory response plays a central role in the pathogenesis of acute lung injury (ALI), the precise molecular mechanisms underlying the development of this disorder remain poorly understood. SOCS3 is an important negative regulator of IL-6-type cytokine signaling. SOCS3 is induced in lung during LPS-induced lung injury, suggesting that generation of SOCS3 may represent a regulatory product during ALI. In the current study, we created mice lacking SOCS3 expression in macrophages and neutrophils (LysM-cre SOCS3(fl/fl)). We evaluated the lung inflammatory response to LPS in both LysM-cre SOCS3(fl/fl) mice and the wild-type (WT) mice (SOCS3(fl/fl)). LysM-cre SOCS3(fl/fl) mice displayed significant increase of the lung permeability index (lung vascular leak of albumin), neutrophils, lung neutrophil accumulation (myeloperoxidase activity), and proinflammatory cytokines/chemokines in bronchial alveolar lavage fluids compared to WT mice. These phenotypes were consistent with morphological evaluation of lung, which showed enhanced inflammatory cell influx and intra-alveolar hemorrhage. We further identify the transcription factor, CCAAT/enhancer-binding protein (C/EBP) δ as a critical downstream target of SOCS3 in LPS-induced ALI. These results indicate that SOCS3 has a protective role in LPS-induced ALI by suppressing C/EBPδ activity in the lung. Elucidating the function of SOCS3 would represent prospective targets for a new generation of drugs needed to treat ALI.
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