Influenza virus aggravates the ox-LDL-induced apoptosis of human endothelial cells via promoting p53 signaling

Suo, Jian; Zhao, Long; Wang, Jian; Zhu, Zhen-Gang; Zhang, Huafeng; Gao, Rong

doi:10.1002/jmv.24166

Cited by 11 publications

(7 citation statements)

References 55 publications

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“…A previous study demonstrated that influenza virus aggravates the ox-LDL-induced apoptosis of human endothelial cells by promoting p53 signaling (35). Infection with A/Porto Rico/8/1934 (H1N1) (PR8) influenza virus in human endothelial EA.hy926 cells induced apoptosis, which was aggravated by ox-LDL treatment.…”

Section: Discussionmentioning

confidence: 99%

Synergistic enhancement of matrix metalloproteinase‑9 expression and pro‑inflammatory cytokines by influenza virus infection and oxidized‑LDL treatment in human endothelial cells

Huang

2017

Exp Ther Med

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Abstract. Oxidized low-density lipoprotein (oxLDL) has been reported to contribute to the development and progression of atherosclerosis, which is also stimulated by viral infections, such as influenza. However, the mechanism underlining the promotion of atherosclerosis by both risk factors remains unclear. In the present study, we investigated the expression of matrix metalloproteinase-9 (MMP-9), which is one of key mediators of atherosclerosis progression, in oxLDL-treated human umbilical vein endothelial cells (HUVEC)-C cells. The infection efficiency of H1N1 pdm2009 influenza virus in the HUVEC-C cells was subsequently examined, and the expression of MMP-9 and proinflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, were determined in the virus-infected HUVEC-C cells, with or without oxLDL treatment. Results demonstrated that oxLDL treatment with 10, 20 or 50 µg/ml markedly upregulated MMP-9 expression at the mRNA and protein levels. H1N1 pdm2009 influenza virus efficiently infected the HUVEC-C cells and significantly promoted the expression of MMP-9, TNF-α, IL-1β and IL-6, synergistically with the oxLDL treatment. Taken together, these results demonstrated for the first time that oxidized-LDL treatment and influenza virus infection synergistically enhance the expression of MMP-9 and proinflammatory cytokines in human endothelial cells, suggesting that both factors are potent stimulators in atherosclerotic impairment to endothelial cells.

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Section: Discussionmentioning

confidence: 99%

Synergistic enhancement of matrix metalloproteinase‑9 expression and pro‑inflammatory cytokines by influenza virus infection and oxidized‑LDL treatment in human endothelial cells

Huang

2017

Exp Ther Med

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“…Both influenza and ox-LDL have been shown to increase apoptosis in vascular endothelial cells, the latter through caspase-9 and caspase-3 cascades (87-91). One study has shown that influenza virus infection synergistically increases ox-LDL-induced apoptosis when compared to apoptosis caused by influenza or ox-LDL alone (97). These influenza-induced effects are possible mechanisms involved in atherosclerotic progression ( Figure 1).…”

Section: Direct Effect Of Influenza On Atherosclerosismentioning

confidence: 99%

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

2020

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Influenza virus infection causes 3-5 million cases of severe illness and 250,000-500,000 deaths worldwide annually. Although pneumonia is the most common complication associated with influenza, there are several reports demonstrating increased risk for cardiovascular diseases. Several clinical case reports, as well as both prospective and retrospective studies, have shown that influenza can trigger cardiovascular events including myocardial infarction (MI), myocarditis, ventricular arrhythmia, and heart failure. A recent study has demonstrated that influenza-infected patients are at highest risk of having MI during the first seven days of diagnosis. Influenza virus infection induces a variety of pro-inflammatory cytokines and chemokines and recruitment of immune cells as part of the host immune response. Understanding the cellular and molecular mechanisms involved in influenza-associated cardiovascular diseases will help to improve treatment plans. This review discusses the direct and indirect effects of influenza virus infection on triggering cardiovascular events. Further, we discussed the similarities and differences in epidemiological and pathogenic mechanisms involved in cardiovascular events associated with coronavirus disease 2019 (COVID-19) compared to influenza infection.

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“…Thus, the permanent status of endothelial activation promoted by these comorbidities would aggravate endothelial dysfunction caused by a viral inflammatory response and could be responsible for the most prevalent fatal outcome described in these patients. 48 Suo and colleagues 49 showed that H1N1pdm09 is responsible for potentiating endothelial cell apoptosis in patients who already have atherosclerosis. In this context, SARS-CoV-2 infection of the pneumocytes, besides having an essential role in the inflammatory activation/dysfunction of endothelial cells, would also lead to endothelial cell death, causing the discontinuity of the alveolar-capillary barrier and facilitating the movement of the virus from the alveolar septum through the alveolar-capillary lumen.…”

Section: Discussionmentioning

confidence: 99%

The Endothelial Dysfunction and Pyroptosis Might Drive the SARS-CoV-2 Lung Injury to the Systemic Immunothrombosis

Nagashima

Mendes²,

Martins

et al. 2020

Preprint

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Objective: Endothelial cells that are close to the alveolar-capillary exchange membranes can be activated by SARS-CoV-2 infection leading to cytokine release and macrophage activation syndrome. This could trigger endothelial dysfunction, pyroptosis, and immunothrombosis, which are the vascular changes commonly referred to as COVID-19 endotheliopathy. Thus, this study aimed to identify tissue biomarkers associated with endothelial activation/dysfunction and the pyroptosis pathway in the lung and myocardial samples of COVID-19 patients and to compare them to pandemic Influenza A virus H1N1 subtype 2009 and Control cases. Approach and Results: Post-mortem lung (COVID-19 group=6 cases; H1N1 group=10 cases, and Control group=11 cases) and myocardial samples (COVID-19=2 cases and control=1 case) were analyzed using immunohistochemistry and the following monoclonal primary antibodies: anti-CD163, anti-interleukin-6 (IL-6), anti-tumor necrosis factor-alpha (TNF-alpha), anti-intercellular adhesion molecule-1 (ICAM-1), and anti-caspase-1. From the result, IL-6, TNF-alpha, ICAM-1, and caspase-1 showed higher tissue expression in the COVID-19 group than in the H1N1 and control groups. Conclusion: Our results demonstrated the presence of endotheliopathy and suggest the participation of the pyroptosis pathway in both the pulmonary and myocardial samples. These conditions might lead to systemic immunothrombotic events that could impair the efforts of clinical staff to avoid fatal outcomes. One of the goals of health professionals should be to identify the high-risk of immunothrombosis patients early to block endotheliopathy and its consequences.

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Influenza virus aggravates the ox-LDL-induced apoptosis of human endothelial cells via promoting p53 signaling

Cited by 11 publications

References 55 publications

Synergistic enhancement of matrix metalloproteinase‑9 expression and pro‑inflammatory cytokines by influenza virus infection and oxidized‑LDL treatment in human endothelial cells

Synergistic enhancement of matrix metalloproteinase‑9 expression and pro‑inflammatory cytokines by influenza virus infection and oxidized‑LDL treatment in human endothelial cells

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

The Endothelial Dysfunction and Pyroptosis Might Drive the SARS-CoV-2 Lung Injury to the Systemic Immunothrombosis

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