ArticleMediators of inflammation2015
Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- SGLT2 inhibitor therapy is associated with IL-10/TGF-α/sVEGFR3 signalling and adipose tissue remodelling in advanced heart failure.Journal of molecular and cellular cardiology plus · 2026Article
- Carbon Monoxide Therapy: Evidence and Prospects for Preventing and Treating Retinal Diseases.Biomolecules · 2026Review
- The Role of Tenascin-C in Neuroinflammation and Neuroplasticity.International journal of molecular sciences · 2025Review
- Carbon monoxide potentiates the effect of corticosteroids in suppressing inflammatory responses in cell culture.Bioorganic & medicinal chemistry · 2025Article
- Endoplasmic Reticulum Stress-Mediated Cell Death in Renal Fibrosis.Biomolecules · 2024Review
- Potentials of ketogenic diet against chronic kidney diseases: pharmacological insights and therapeutic prospects.Molecular biology reports · 2022Review
- Identification of Cytoprotective Small-Molecule Inducers of Heme-Oxygenase-1.Antioxidants (Basel, Switzerland) · 2022Article
- Carbon monoxide-releasing molecule-2 protects intestinal mucosal barrier function by reducing epithelial tight-junction damage in rats undergoing cardiopulmonary resuscitation.Journal of intensive medicine · 2022Article
- Tenascin-C Participates Pulmonary Injury Induced by Paraquat Through Regulating TLR4 and TGF-β Signaling Pathways.Inflammation · 2022Article
- Tenascin C Has a Modest Protective Effect on Acute Lung Pathology during Methicillin-Resistant Staphylococcus aureus-Induced Pneumonia in Mice.Microbiology spectrum · 2021Article
- Nature's marvels endowed in gaseous molecules I: Carbon monoxide and its physiological and therapeutic roles.Acta pharmaceutica Sinica. B · 2021Review
- Amelioration of Murine Macrophage Activation Syndrome by Monomethyl Fumarate in Both a Heme Oxygenase 1-Dependent and Heme Oxygenase 1-Independent Manner.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Pharmacotherapy against Oxidative Stress in Chronic Kidney Disease: Promising Small Molecule Natural Products Targeting Nrf2-HO-1 Signaling.Antioxidants (Basel, Switzerland) · 2021Review
- CO-Releasing Molecule-2 Prevents Acute Kidney Injury through Suppression of ROS-Fyn-ER Stress Signaling in Mouse Model.Oxidative medicine and cellular longevity · 2021Article
- Tenascin-C Deficiency Is Associated With Reduced Bacterial Outgrowth DuringFrontiers in immunology · 2021Article
- Carbon monoxide: An emerging therapy for acute kidney injury.Medicinal research reviews · 2020Review
- Targeting the Heme Oxygenase 1/Carbon Monoxide Pathway to Resolve Lung Hyper-Inflammation and Restore a Regulated Immune Response in Cystic Fibrosis.Frontiers in pharmacology · 2020Review
- Clinical significance and prognosis of serum tenascin-C in patients with sepsis.BMC anesthesiology · 2018Article
- Stanniocalcin-2 contributes to mesenchymal stromal cells attenuating murine contact hypersensitivity mainly via reducing CD8Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, is specifically induced upon tissue injury and infection and during septic conditions. Carbon monoxide (CO) gas is known to exert various anti-inflammatory effects in various inflammatory diseases. However, the mechanisms underlying the effect of CO on TN-C-mediated inflammation are unknown. In the present study, we found that treatment with LPS significantly enhanced TN-C expression in macrophages. CO gas, or treatment with the CO-donor compound, CORM-2, dramatically reduced LPS-induced expression of TN-C and proinflammatory cytokines while significantly increased the expression of IL-10. Treatment with TN-C siRNA significantly suppressed the effects of LPS on proinflammatory cytokines production. TN-C siRNA did not affect the CORM-2-dependent increase of IL-10 expression. In cells transfected with IL-10 siRNA, CORM-2 had no effect on the LPS-induced expression of TN-C and its downstream cytokines. These data suggest that IL-10 mediates the inhibitory effect of CO on TN-C and the downstream production of proinflammatory cytokines. Additionally, administration of CORM-2 dramatically reduced LPS-induced TN-C and proinflammatory cytokines production while expression of IL-10 was significantly increased. In conclusion, CO regulated IL-10 expression and thus inhibited TN-C-mediated inflammation in vitro and in vivo.
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