ArticlePloS one2014
Involvement of the Akt/NF-κB pathways in the HTNV-mediated increase of IL-6, CCL5, ICAM-1, and VCAM-1 in HUVECs.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Forkhead box O3 transcription factor fine-tunes IL-6 expression in mycobacteria-infected macrophages.Frontiers in immunology · 2026Article
- IL-6 trans-signaling mediates cytokine secretion and barrier dysfunction in hantavirus-infected cells and correlates to severity in HFRS.PLoS pathogens · 2025Article
- Plasma thrombomodulin is a valuable biomarker to predict the severity of hemorrhagic fever with renal syndrome caused by the Hantaan virus.Frontiers in cellular and infection microbiology · 2025Article
- Cardamonin decreases inflammatory mediator expression in IL-1β-stimulated human periodontal ligament cells.Molecular biology reports · 2024Article
- Disparate macrophage responses are linked to infection outcome of Hantan virus in humans or rodents.Nature communications · 2024Article
- Hemorrhagic fever with renal syndrome caused by destruction of residential area of rodent in a construction site: epidemiological investigation.BMC infectious diseases · 2022Article
- Article
- Ethanolic extract of Artemisia campestris subsp. glutinosa (Besser) Batt. inhibits HIV-1 replication in vitro through the activity of terpenes and flavonoids on viral entry and NF-κB pathway.Journal of ethnopharmacology · 2020Article
- Investigation on risk factors of haemorrhagic fever with renal syndrome (HFRS) in Xuancheng City in Anhui Province, Mainland China.Epidemiology and infection · 2020Article
- RNA-Seq Revealed a Circular RNA-microRNA-mRNA Regulatory Network in Hantaan Virus Infection.Frontiers in cellular and infection microbiology · 2020Review
- Hantavirus infection: a global zoonotic challenge.Virologica Sinica · 2017Review
- Review
- Interferon-Induced Transmembrane Protein 3 Inhibits Hantaan Virus Infection, and Its Single Nucleotide Polymorphism rs12252 Influences the Severity of Hemorrhagic Fever with Renal Syndrome.Frontiers in immunology · 2016Article
- Aging-associated oxidized albumin promotes cellular senescence and endothelial damage.Clinical interventions in aging · 2016Article
- Hemorrhagic Fever with Renal Syndrome: Pathogenesis and Clinical Picture.Frontiers in cellular and infection microbiology · 2016Review
- Article
- IL-33/ST2 correlates with severity of haemorrhagic fever with renal syndrome and regulates the inflammatory response in Hantaan virus-infected endothelial cells.PLoS neglected tropical diseases · 2015Article
- Hantavirus-induced disruption of the endothelial barrier: neutrophils are on the payroll.Frontiers in microbiology · 2015Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHantaan virus (HTNV) infection causes a severe form of HFRS(hemorrhagic fever with renal syndrome)in Asia. Although HTNV has been isolated for nearly forty years, the pathogenesis of HFRS is still unknown, and little is known regarding the signaling pathway that is activated by the virus. METHODOLOGY/PRINCIPAL
findingsCardamonin was selected as a NF-κB inhibitor, and indirect immunofluorescence assays were used to detect the effect of cardamonin on HTNV-infected HUVECs. The effect of cardamonin on the HTNV-induced phosphorylation of Akt and DNA-binding activity of NF-κB were determined using Western blot analysis and electrophoretic mobility shift assays (EMSAs), respectively. Then, flow cytometric and quantitative real-time PCR analyses were performed to quantify the expression levels of the adhesion molecules ICAM-1 and VCAM-1, and the concentrations of IL-6, IL-8, and CCL5 in HUVEC supernatants were examined using ELISA. The results showed that cardamonin did not effect the proliferation of HUVECs or the replication of HTNV in HUVECs. Instead, cardamonin inhibited the phosphorylation of Akt and nuclear transduction of NF-κB and further reduced the expression of the adhesion molecules ICAM-1 and VCAM-1 in HTNV-infected HUVECs. Cardamonin also inhibited the secretion of IL-6 and CCL5, but not IL-8. CONCLUSION/SIGNIFICANCE: HTNV replication may not be dependent upon the ability of the virus to activate NF-κB in HUVECs. The Akt/NF-κB pathways may be involved in the pathogenesis of HFRS; therefore, cardamonin may serve as a potential beneficial agent for HFRS therapy.
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