ArticleJournal of inflammation (London, England)2017
Successful reduction of inflammatory responses and arachidonic acid-cyclooxygenase 2 pathway in human pulmonary artery endothelial cells by silencing adipocyte fatty acid-binding protein.
Article in Journal of inflammation (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Nephron-associated Support Cell Transcriptional Plasticity Expands in Hypertension.bioRxiv : the preprint server for biology · 2026Article
- Deciphering the anti-atherosclerotic mechanisms of Danggui-Chuanxiong herb pair: a synergistic approach combining computational prediction andFrontiers in cardiovascular medicine · 2026Article
- Fatty Acid-Binding Protein 4 Inhibition Promotes Locomotor and Autonomic Recovery in Rats following Spinal Cord Injury.Journal of neurotrauma · 2022Article
- MUC16 facilitates cervical cancer progression via JAK2/STAT3 phosphorylation-mediated cyclooxygenase-2 expression.Genes & genomics · 2020Article
- The Anti-inflammatory Effect of Soluble Epoxide Hydrolase Inhibitor and 14, 15-EET in Kawasaki Disease Through PPARγ/STAT1 Signaling Pathway.Frontiers in pediatrics · 2020Article
- Fatty Acid-Binding Protein 4 in Cardiovascular and Metabolic Diseases.Journal of atherosclerosis and thrombosis · 2019Review
- [miR-203 inhibits lung cancer cell metastasis by targeting fatty acid binding protein 4].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdipocyte fatty acid-binding protein, also known as aP2 or fatty acid-binding protein 4 (FABP4), plays an important role in inflammatory and metabolic responses in adipocytes and macrophages. Recent work has demonstrated that macrophage FABP4 integrates inflammatory and lipid metabolic responses, thereby contributing to the development of insulin resistance and atherosclerosis. However, it is not known whether FABP4 in human pulmonary artery endothelial cells(HPAECs) modulates inflammation.
resultsHere, we demonstrate that FABP4 and inflammatory cytokines are upregulated in lipopolysaccharide(LPS)-stimulated HPAECs. In addition, LPS increases the expression of molecules in the arachidonic acid(AA)-cyclooxygenase (COX) 2 signaling pathway in FABP4-expressing, but not FABP4-deficient, HPAECs.
conclusionsOur findings demonstrate that silencing FABP4 could decrease inflammatory cytokines, which were reported to be expressed via the AA-COX2 pathway, in HPAECs. In addition, silencing FABP4 could inhibit the expression of molecules in the AA-COX2 pathways. So we speculate silencing FABP4 could decrease the inflammatory response in HPAECs, which involves in the AA-COX2 signaling pathway. Our study suggests that FABP4 could be a potential biomarker and intervention point for the inflammation-related disease in HPAECs such as pulmonary thromboembolism.
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