ArticleActa pharmacologica Sinica2014
TNF-α induces CXCL1 chemokine expression and release in human vascular endothelial cells in vitro via two distinct signaling pathways.
Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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49 citing papers in PubMed, 87 citations in OpenAlex.
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- CXCL-CXCR2 signaling drives cancer-endothelium interactions in SCLC metastatic seeding.bioRxiv : the preprint server for biology · 2026Article
- P2X7 and inflammatory fingerprinting of patients with carotid atherosclerosis and the risk of abdominal aortic aneurysm.Scientific reports · 2025Article
- TGFβ1-TNFα-regulated secretion of neutrophil chemokines is independent of epithelial-mesenchymal transition in breast tumor cells.Molecular biology of the cell · 2025Article
- Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.Molecular and cellular biochemistry · 2025Review
- Construction and validation of a chemokine-related gene signature associated with prognosis, clinical significance, and immune microenvironment characteristics in cervical cancer.Discover oncology · 2025Article
- Repeated Low-Level Inflammatory Challenge Leads to Alterations in the TNF-CXCL10 Signalling Pathway in Mouse Cerebral Endothelial Cells In Vitro.Journal of neurochemistry · 2025Article
- NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain.Journal of neuroinflammation · 2025Article
- The Role of TNF-α in Neuropathic Pain: An Immunotherapeutic Perspective.Life (Basel, Switzerland) · 2025Review
- Endothelial-Mesenchymal Transition and Possible Role of Cytokines in Streptozotocin-Induced Diabetic Heart.Biomedicines · 2025Article
- Smad4 deficiency in hepatocytes attenuates NAFLD progression via inhibition of lipogenesis and macrophage polarization.Cell death & disease · 2025Article
- Derivation of novel metabolic pathway score identifies alanine metabolism as a targetable influencer of TNF-alpha signaling.Heliyon · 2024Article
- The Clinical Significance and Involvement in Molecular Cancer Processes of Chemokine CXCL1 in Selected Tumors.International journal of molecular sciences · 2024Review
- Self-assembled and perfusable microvasculature-on-chip for modeling leukocyte trafficking.Lab on a chip · 2024Article
- Article
- In silico based analysis to explore genetic linkage between atherosclerosis and its potential risk factors.Biochemistry and biophysics reports · 2023Article
- Effects of whole-brain radiation therapy on the blood-brain barrier in immunocompetent and immunocompromised mouse models.Radiation oncology (London, England) · 2023Article
- Pathogenesis of Anemia in Canine Babesiosis: Possible Contribution of Pro-Inflammatory Cytokines and Chemokines-A Review.Pathogens (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
aimChemokines usually direct the movement of circulating leukocytes to sites of inflammation or injury. CXCL1/GRO-α has been shown to be upregulated in atherosclerotic lesions and various cancers. The aim of this study was to investigate the mechanisms underlying the TNF-α-induced release of CXCL1 from human vascular endothelial cells in vitro.
methodsHuman umbilical vein endothelial cells (HUVECs) were treated with different proinflam-matory mediators and growth factors. CXCL1 expression and secretion were determined using RT-PCR and ELISA, respectively. TNF-α-induced cell signaling was assayed with Western blotting. Cell viability/growth was determined using MTT assay. Monocyte migration was measured with transwell migration assay.
resultsAmong the 17 mediators and growth factors tested, TNF-α, LPS and thrombin induced marked increase in CXCL1 release from HUVEC cells. TNF-α (2, 5 ng/mL) induced CXCL1 release and mRNA expression in the cells in concentration- and time-dependent manners. TNF-α (5 ng/mL) caused activation of JNK, p38 MAPK, PI3K and Akt, whereas pretreatment with JNK inhibitor (SP600125), p38 MAPK inhibitor (SB202190) or PI-3K inhibitor (LY294002) significantly suppressed TNF-α-induced CXCL1 release from the cells. But only SP600125 significantly reduced TNF-α-induced CXCL1 mRNA expression in the cells. Moreover, dexamethasone (up to 500 nmol/L) failed to affect TNF-α-induced CXCL1 release from the cells. In functional studies, recombinant CXCL1 enhanced HUVEC proliferation, and both recombinant CXCL1 and TNF-α-induced CXCL1 from HUVECs attracted human monocyte migration.
conclusionTNF-α stimulates CXCL1 release from human ECs through JNK-mediated CXCL1 mRNA expression and p38 MAPK- and PI-3K-mediated CXCL1 secretory processes.
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