ArticleActa biochimica et biophysica Sinica2017
Recombinant CC16 protein inhibits the production of pro-inflammatory cytokines via NF-κB and p38 MAPK pathways in LPS-activated RAW264.7 macrophages.
Article in Acta biochimica et biophysica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Impaired CC16-mediated host responses to rhinovirus in nasal epithelial cells from patients with asthma.The Journal of allergy and clinical immunology · 2026Article
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- Club cell secretory protein 16 promotes cell proliferation and inhibits inflammation and pyroptosis in response to particulate matter 2.5-induced epithelial damage in asthmatic mice.Journal of thoracic disease · 2025Article
- Dynamics of the blood plasma proteome during hyperacute HIV-1 infection.Nature communications · 2024Article
- Preliminary proteomic analysis of mouse lung tissue treated with cyclophosphamide and Venetin-1.Scientific reports · 2024Article
- Sivelestat protects against acute lung injury by up-regulating angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas receptors.Journal of thoracic disease · 2024Article
- Club Cells-A Guardian against Occupational Hazards.Biomedicines · 2023Review
- Article
- Extracellular vesicle-encapsulated CC16 as novel nanotherapeutics for treatment of acute lung injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Relationships of serum CC16 levels with smoking status and lung function in COPD.Respiratory research · 2022Article
- Neobavaisoflavone ameliorates LPS-induced RAW264.7 cell inflammations by suppressing the activation of NF-κB and MAPKs signaling pathways.Iranian journal of basic medical sciences · 2022Article
- The traditional Chinese patented medicine Qingke Pingchuan granules alleviate acute lung injury by regenerating club cells.Pulmonary circulation · 2022Article
- Utilising Network Pharmacology to Explore Underlying Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- The Involvement of PDE4 in the Protective Effects of Melatonin on Cigarette-Smoke-Induced Chronic Obstructive Pulmonary Disease.Molecules (Basel, Switzerland) · 2021Article
- CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells duringInternational journal of molecular sciences · 2021Article
- Destruction of Neutrophil Extracellular Traps Promotes the Apoptosis and Inhibits the Invasion of Gastric Cancer Cells by Regulating the Expression of Bcl-2, Bax and NF-κB.OncoTargets and therapy · 2020Article
- Recombinant CC16 inhibits NLRP3/caspase-1-induced pyroptosis through p38 MAPK and ERK signaling pathways in the brain of a neonatal rat model with sepsis.Journal of neuroinflammation · 2019Article
- Club cell protein 16 in sera from trauma patients modulates neutrophil migration and functionality via CXCR1 and CXCR2.Molecular medicine (Cambridge, Mass.) · 2019Article
- Retracted Article: Anti-inflammatory potency ofRSC advances · 2019Article
- ANKRD49 inhibits etoposide-induced intrinsic apoptosis of GC-1 cells by modulating NF-κB signaling.Molecular and cellular biochemistry · 2019Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates that Clara cell protein-16 (CC16) has anti-inflammatory functions, although the involved molecular pathways have not been completely elucidated. Here, we evaluated the effect of recombinant rat CC16 (rCC16) on the expression of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-8 in lipopolysaccharide (LPS)-stimulated mouse macrophages (RAW264.7 cells) and explored the underlying molecular mechanisms. It was found that rCC16 inhibited LPS-induced TNF-α, IL-6, and IL-8 expression at both the messenger ribonucleicacid (mRNA) level and protein level in a concentration-dependent manner, as demonstrated by real-time reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay. Such suppressive effects were accompanied by the inhibition of transcriptional activity and the deoxyribonucleic acid binding activity of nuclear factor (NF)-κB but not activator protein (AP)-1. Western blot analysis further revealed that rCC16 inhibited the increase of nuclear NF-κB and the reduction of cytosolic NF-κB, the phosphorylation and reduction of NF-κB inhibitory protein IκBα, and the p38 mitogen-activated protein kinase (MAPK)-dependent NF-κB activation by phosphorylation at Ser276 of its p65 subunit. Furthermore, rCC16 was found to have no effect on the phosphorylation of c-Jun N-terminal kinase, c-Jun, or the nuclear translocation of c-Jun. In addition, reduction of TNF-α, IL-6, and IL-8 were reversed when the level of endogenous uteroglobin-binding protein was reduced by RNA interference in rCC16- and LPS-treated RAW264.7 cells. Our data suggest that rCC16 suppresses LPS-mediated inflammatory mediator TNF-α, IL-6, and IL-8 production by inactivating NF-κB and p38 MAPK but not AP-1 in RAW264.7 cells.
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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.