ArticleInflammation2017
Regulation of iNOS-Derived ROS Generation by HSP90 and Cav-1 in Porcine Reproductive and Respiratory Syndrome Virus-Infected Swine Lung Injury.
Article in Inflammation, 2017. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- PRRSV infection induces mitochondrial damage and releases mitochondrial dsRNA to activate the NLRP3-dependent inflammatory response.Veterinary research · 2026Article
- Differential Effects of Selenium Compounds on Mitochondrial Function in PRRSV-Infected Porcine Alveolar Macrophages.Viruses · 2025Article
- Mitochondrial dysfunction in PRRSV-2-infected macrophages.Frontiers in immunology · 2025Article
- Cinnamaldehyde Protects againstInternational journal of molecular sciences · 2024Article
- Effect of tubastatin A on NLRP3 inflammasome activation in macrophages under hypoxia/reoxygenation conditions.World journal of emergency medicine · 2024Article
- Target Discovery of Matrine against PRRSV in Marc-145 Cells via Activity-Based Protein Profiling.International journal of molecular sciences · 2023Article
- Innate and Adaptive Immune Responses Induced by Aspergillus fumigatus Conidia and Hyphae.Current microbiology · 2022Article
- AMP-activated kinase regulates porcine reproductive and respiratory syndrome virus infection in vitro.Virus genes · 2022Article
- Porphyromonas gingivalis infection alters Nrf2-phase II enzymes and nitric oxide in primary human aortic endothelial cells.Journal of periodontology · 2021Article
- Differential responses in placenta and fetal thymus at 12 days post infection elucidate mechanisms of viral level and fetal compromise following PRRSV2 infection.BMC genomics · 2020Article
- Susceptibility of porcine pulmonary microvascular endothelial cells to porcine reproductive and respiratory syndrome virus.The Journal of veterinary medical science · 2020Article
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
- Activation of pro- and anti-inflammatory responses in lung tissue injury during the acute phase of PRRSV-1 infection with the virulent strain Lena.Veterinary microbiology · 2020Article
- Review
- Signaling pathways involved in regulating apoptosis induction in host cells upon PRRSV infection.Virus genes · 2019Review
- Porphyromonas gingivalis induced inflammatory responses and promoted apoptosis in lung epithelial cells infected with H1N1 via the Bcl‑2/Bax/Caspase‑3 signaling pathway.Molecular medicine reports · 2018Article
- Impact of PRRSV infection and dietary soybean meal on ileal amino acid digestibility and endogenous amino acid losses in growing pigs.Journal of animal science · 2018Article
- Arsenic and/or copper caused inflammatory response via activation of inducible nitric oxide synthase pathway and triggered heat shock protein responses in testis tissues of chicken.Environmental science and pollution research international · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the lungs, endothelial nitric oxide synthase (eNOS) is usually expressed in endothelial cells and inducible nitric oxide synthase (iNOS) is mainly expressed in alveolar macrophages and epithelial cells. Both eNOS and iNOS are involved in lung inflammation. While they play several roles in lung inflammation formation and resolution, their expression and activity are also regulated by inflammatory factors. Their expression relationship in virus infection-induced lung injury is not well addressed. In this report, we analyzed expression of both eNOS and iNOS, the production of nitric oxide (NO) and reactive oxygen species (ROS), and expression of their associated regulatory proteins, heat shock protein 90 (HSP90) and caveolin-1 (Cav-1), in a swine lung injury model induced by porcine reproductive and respiratory syndrome virus (PRRSV) infection. The combination of upregulation of iNOS and downregulation of eNOS was observed in both natural and experimental PRRSV-infected lungs, while the combination is much enhanced in natural infected lungs. While NO production is much reduced in both infections, ROS was enhanced only in natural infected lungs. Moreover, HSP90 is increased in both natural and experimental infection and less Cav-1 expressed was observed only in the natural PRRSV-infected lungs. Therefore, the increased ROS generation is likely due to the increased iNOS and its unbalanced regulation by HSP90 and Cav-1, and it also likely causes higher endothelial dysfunction in clinical PRRSV-infected lungs.
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Registered trials
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