Endothelial Cell Contributions to COVID-19

Oxford, Alexandra E.; Halla, Fabio; Robertson, Evan B.; Morrison, Brad

doi:10.3390/pathogens9100785

Cited by 17 publications

(11 citation statements)

References 78 publications

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“…In humans, direct vascular endothelial cell infection and resulting vasculitis have been reported [29]. Although ACE2 is also widely expressed on epithelial cells as on pneumocytes, it is currently ambiguous why the virus replicates better in respiratory tracts than in vascular endothelial cells [30]. To prove this, other SARS-CoV-2 receptors on the surface of human cells have been suggested, such as transmembrane serine protease 2, sialic acid, and extracellular matrix metalloproteinase inducer [31].…”

Section: Discussionmentioning

confidence: 99%

Ultra- and micro-structural changes of respiratory tracts in SARS-CoV-2 infected Syrian hamsters

Yang

et al. 2021

Vet Res

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The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic is causing a global crisis. It is still unresolved. Although many therapies and vaccines are being studied, they are still in their infancy. As this pandemic continues, rapid and accurate research for the development of therapies and vaccines is needed. Therefore, it is necessary to understand characteristics of diseases caused by SARS-CoV-2 through animal models. Syrian hamsters are known to be susceptible to SARS-CoV-2. They were intranasally inoculated with SARS-CoV-2. At 2, 4, 8, 12, and 16 days post-infection (dpi), these hamsters were euthanized, and tissues were collected for ultrastructural and microstructural examinations. Microscopic lesions were prominent in the upper and lower respiratory tracts from 2 and 4 dpi groups, respectively. The respiratory epithelium in the trachea, bronchiole, and alveolar showed pathological changes. Inflammatory cells including neutrophils, lymphocytes, macrophages, and eosinophils were infiltrated in/around tracheal lamina propria, pulmonary vessels, alveoli, and bronchiole. In pulmonary lesions, alveolar wall was thickened with infiltrated inflammatory cells, mainly neutrophils and macrophages. In the trachea, epithelial damages started from 2 dpi and recovered from 8 dpi, consistent with microscopic results, High levels of SARS-CoV-2 nucleoprotein were detected at 2 dpi and 4 dpi. In the lung, lesions were most severe at 8 dpi. Meanwhile, high levels of SARS-CoV-2 were detected at 4 dpi. Electron microscopic examinations revealed cellular changes in the trachea epithelium and alveolar epithelium such as vacuolation, sparse micro-organelle, and poor cellular margin. In the trachea epithelium, the number of cytoplasmic organelles was diminished, and small vesicles were prominent from 2 dpi. Some of these electron-lucent vesicles were filled with virion particles. From 8 dpi, the trachea epithelium started to recover. Because of shrunken nucleus and swollen cytoplasm, the N/C ratio of type 2 pneumocyte decreased at 8 and 12 dpi. From 8 dpi, lamellar bodies on type 2 pneumocyte cytoplasm were increasingly observed. Their number then decreased from 16 dpi. However, there was no significant change in type 1 pneumocyte. Viral vesicles were only observed in the cytoplasm of type 2 pneumocyte. In conclusion, ultra- and micro-structural changes presented in this study may provide useful information for SARS-CoV-2 studies in various fields.

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Section: Discussionmentioning

confidence: 99%

Ultra- and micro-structural changes of respiratory tracts in SARS-CoV-2 infected Syrian hamsters

Yang

et al. 2021

Vet Res

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“…The profound inflammatory response to SARS-CoV-2 infection leads to the development of coagulation abnormalities 146 . Vascular endothelial dysfunction seems to contribute to the pathophysiology of microcirculatory changes in patients with SARS-CoV-2 infection 149 . Importantly, SARS-CoV-2 can enter and infect endothelial cells via the ACE2 receptor 150 , with viral replication causing inflammatory cell infiltration, endothelial cell apoptosis and microvascular prothrombotic effects 151 .…”

Section: Thromboembolic Eventsmentioning

confidence: 99%

COVID-19 and diabetes mellitus: from pathophysiology to clinical management

et al. 2020

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Initial studies found increased severity of coronavirus disease 2019 (COVID-19), caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in patients with diabetes mellitus. Furthermore, COVID-19 might also predispose infected individuals to hyperglycaemia. Interacting with other risk factors, hyperglycaemia might modulate immune and inflammatory responses, thus predisposing patients to severe COVID-19 and possible lethal outcomes. Angiotensin-converting enzyme 2 (ACE2), which is part of the renin–angiotensin–aldosterone system (RAAS), is the main entry receptor for SARS-CoV-2; although dipeptidyl peptidase 4 (DPP4) might also act as a binding target. Preliminary data, however, do not suggest a notable effect of glucose-lowering DPP4 inhibitors on SARS-CoV-2 susceptibility. Owing to their pharmacological characteristics, sodium–glucose cotransporter 2 (SGLT2) inhibitors might cause adverse effects in patients with COVID-19 and so cannot be recommended. Currently, insulin should be the main approach to the control of acute glycaemia. Most available evidence does not distinguish between the major types of diabetes mellitus and is related to type 2 diabetes mellitus owing to its high prevalence. However, some limited evidence is now available on type 1 diabetes mellitus and COVID-19. Most of these conclusions are preliminary, and further investigation of the optimal management in patients with diabetes mellitus is warranted.

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“…COVID-19 infection caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was shown to be associated with endothelial dysfunction manifested as increased formation of micro-thrombi, cytokine production by endothelium and deregulated immune responses [ 181 ]. Endothelial cells reportedly express both ACE2 and TMPRSS2 which makes them susceptible to direct viral entry and infection.…”

Section: The Biological and Clinical Relevance Of Endothelial Evs In Covid-19mentioning

confidence: 99%

Endothelial Extracellular Vesicles: From Keepers of Health to Messengers of Disease

Mathiesen

Hamilton

Carter

et al. 2021

IJMS

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Endothelium has a rich vesicular network that allows the exchange of macromolecules between blood and parenchymal cells. This feature of endothelial cells, along with their polarized secretory machinery, makes them the second major contributor, after platelets, to the particulate secretome in circulation. Extracellular vesicles (EVs) produced by the endothelial cells mirror the remarkable molecular heterogeneity of their parent cells. Cargo molecules carried by EVs were shown to contribute to the physiological functions of endothelium and may support the plasticity and adaptation of endothelial cells in a paracrine manner. Endothelium-derived vesicles can also contribute to the pathogenesis of cardiovascular disease or can serve as prognostic or diagnostic biomarkers. Finally, endothelium-derived EVs can be used as therapeutic tools to target endothelium for drug delivery or target stromal cells via the endothelial cells. In this review we revisit the recent evidence on the heterogeneity and plasticity of endothelial cells and their EVs. We discuss the role of endothelial EVs in the maintenance of vascular homeostasis along with their contributions to endothelial adaptation and dysfunction. Finally, we evaluate the potential of endothelial EVs as disease biomarkers and their leverage as therapeutic tools.

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Endothelial Cell Contributions to COVID-19

Cited by 17 publications

References 78 publications

Ultra- and micro-structural changes of respiratory tracts in SARS-CoV-2 infected Syrian hamsters

Ultra- and micro-structural changes of respiratory tracts in SARS-CoV-2 infected Syrian hamsters

COVID-19 and diabetes mellitus: from pathophysiology to clinical management

Endothelial Extracellular Vesicles: From Keepers of Health to Messengers of Disease

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