ArticleCell biology and toxicology2018
Lipopolysaccharide-induced CCN1 production enhances interleukin-6 secretion in bronchial epithelial cells.
Article in Cell biology and toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- A photonic biosensor-integrated tissue chip platform for real-time sensing of lung epithelial inflammatory markers.Lab on a chip · 2023Article
- The CREB and AP-1-Dependent Cell Communication Network Factor 1 Regulates Porcine Epidemic Diarrhea Virus-Induced Cell Apoptosis Inhibiting Virus Replication Through the p53 Pathway.Frontiers in microbiology · 2022Article
- Penehyclidine hydrochloride alleviates lipopolysaccharide‑induced acute respiratory distress syndrome in cells via regulating autophagy‑related pathway.Molecular medicine reports · 2021Article
- Extracellular Vesicles and Alveolar Epithelial-Capillary Barrier Disruption in Acute Respiratory Distress Syndrome: Pathophysiological Role and Therapeutic Potential.Frontiers in physiology · 2021Review
- Article
- Mechanisms of interactions between lung-origin telocytes and mesenchymal stem cells to treat experimental acute lung injury.Clinical and translational medicine · 2020Article
- SARS-CoV-2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- The Roles of CCN1/CYR61 in Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Evidence for the critical role of the PI3K signaling pathway in particulate matter-induced dysregulation of the inflammatory mediators COX-2/PGECell biology and toxicology · 2020Article
- Regulatory mechanism of NOV/CCN3 in the inflammation and apoptosis of lung epithelial alveolar cells upon lipopolysaccharide stimulation.Molecular medicine reports · 2020Article
- Molecular regulation and clinical significance of caveolin-1 methylation in chronic lung diseases.Clinical and translational medicine · 2020Review
- Roles of transforming growth factor-β and phosphatidylinositol 3-kinase isoforms in integrin β1-mediated bio-behaviors of mouse lung telocytes.Journal of translational medicine · 2019Article
- Interferon gamma induces inflammatory responses through the interaction of CEACAM1 and PI3K in airway epithelial cells.Journal of translational medicine · 2019Article
- Predictors of circulating INTERLEUKIN-6 levels in head and neck cancer patients.Cancers of the head & neck · 2018Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a clinical complication caused by primary or secondary lung injury, as well as by systemic inflammation. Researches regarding molecular pathophysiology of ALI/ARDS are immerging with an ultimate aim towards developing prognostic molecular biomarkers and molecule-based therapy. However, the molecular mechanisms concerning ALI/ARDS are still not completely understood. The purpose of the present study was to identify a crucial role of CCN1 in inflammatory microenvironment during ALI/ARDS and focus on a potential communication between CCN1 and interleukin-6 (IL-6) in the airway epithelial cells. Our data illustrated that the expression levels of CCN1 and IL-6 in bronchoalveolar lavage fluid (BALF) in a lipopolysaccharide (LPS)-induced ALI mouse model were significantly elevated and the pulmonary expression of CCN1 was restricted to bronchial epithelial cells. Interestingly, both endogenous and exogenous CCN1 stimulated IL-6 production in vitro. Furthermore, LPS-induced IL-6 production in a bronchial epithelial cell line was blocked by CCN siRNA whereas CCN1 induced by LPS was sensitive to PI3K inhibition. Together, our data indicate a linear signal pathway, LPS-CCN1-IL-6, existing in bronchial epithelial cells after LPS exposure. This finding may represent an additional mechanism and a novel target for development of therapy and biomarker on ALI/ARDS.
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