ArticleFrontiers in pharmacology2020
The rCC16 Protein Protects Against LPS-Induced Cell Apoptosis and Inflammatory Responses in Human Lung Pneumocytes.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 21 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
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- 6β-Acetoxysandaracopimaradien-1α,9α-diol Attenuates LPS-Induced Acute Lung Injury: Association with Alterations in Src, MAPK, and Akt/GSK-3β Signalling.International journal of molecular sciences · 2026Article
- The role of CC16 in the associations of preterm birth with lung function and asthma in adult life.The Journal of allergy and clinical immunology · 2026Article
- Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- 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
- Clara cell secretory protein 16 protects against PM2.5-induced ferroptosis in mouse lung epithelial cells in a concentration-dependent manner.American journal of translational research · 2025Article
- Contrasting the clinical and biological characteristics of young and old COPD patients.ERJ open research · 2025Article
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- 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
- Article
- MicroRNA-155-5p modulates the progression of acute respiratory distress syndrome by targeting interleukin receptors.Bioengineered · 2022Article
- Network pharmacology and molecular docking analysis reveals the mechanism of asiaticoside on COVID-19.Annals of translational medicine · 2022Article
- Herbo-mineral formulation, Divya-Swasari-Vati averts SARS-CoV-2 pseudovirus entry into human alveolar epithelial cells by interfering with spike protein-ACE 2 interaction and IL-6/TNF-α /NF-κB signaling.Frontiers in pharmacology · 2022Article
- Classic Signaling Pathways in Alveolar Injury and Repair Involved in Sepsis-Induced ALI/ARDS: New Research Progress and Prospect.Disease markers · 2022Review
- Deciphering the Active Compounds and Mechanisms of HSBDF for Treating ALIFrontiers in pharmacology · 2022Article
- CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells duringInternational journal of molecular sciences · 2021Article
- Article
- CD39Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOur previous clinical study showed that low lung levels of CC16 strongly influence the occurrence and development of ARDS. The aim of the present study was to evaluate the therapeutic effect of rCC16 on LPS-induced inflammation in A549 cells and to determine its mechanism.
methodsCell apoptosis and inflammation was induced by LPS stimulation. The cytotoxic effect of rCC16 was evaluated using the MTT assay. Cytokine levels were determined using enzyme-linked immunosorbent assays. The molecular mechanism of rCC16 was investigated by analyzing relevant signaling pathways.
resultsThe LPS treatment of A549 cells significantly decreased cell viability, increased the levels of the apoptotic proteins Bax, Bak and Cleaved Caspase-3, the secretion of inflammatory cytokines, and the expression levels of TLR4, p-NF/κB, MAPK proteins. While the levels of Bcl-2, p-AKT, p-mTOR, p-ERK1/2, NF/κB, p-AMPK, and p-p38 were significantly decreased in LPS-treated A549 cells. Our experimental results also confirmed that rCC16 inhibited LPS-induced apoptosis, promoted A549 cell proliferation by activating the PI3K/AKT/mTOR/ERK1/2 pathway, and inhibited the release of certain inflammatory factors, especially HMGB1, through dephosphorylation and inactivation of the TLR4/NF-κB/AMPK signaling pathways.
conclusionThese results highlight the potential utility of CC16 as an important cytokine for the prevention or treatment of inflammation and show that CC16 may play an important role in the future clinical treatment of ARDS.
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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.