Dynamic Regulation of SARS-Cov-2 Binding and Cell Entry Mechanisms in Remodeled Human Ventricular Myocardium

Bristow, Michael R.; Zisman, Lawrence S.; Altman, Natasha; Gilbert, Edward M.; Lowes, Brian D.; Minobe, Wayne; Slavov, Dobromir; Schwisow, Jessica A.; Rodríguez, Erin M.; Carroll, Ian A.; Keuer, Thomas A.; Buttrick, Peter M.; Kao, David

doi:10.1016/j.jacbts.2020.06.007

Cited by 48 publications

(45 citation statements)

References 55 publications

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“…Significantly, short-ACE2 is missing the aminoacidic residues reported as fundamental for virus binding; however, due to the lack of detailed data regarding its function we cannot exclude that the short-ACE2 may modulate SARS-CoV-2 susceptibility by interacting with long-ACE2 or additional membrane proteins which may mediate the binding to SARS-CoV-2 spike protein [e.g. ITGA5, as previously observed (60)]. Of interest, nasal epithelium, reported to represent the main reservoir of SARS-CoV-2 (61), showed higher levels of short-ACE2 vs. long-ACE2 (24).…”

Section: Discussionmentioning

confidence: 88%

SARS-CoV-2 receptor Angiotensin I-Converting Enzyme type 2 (ACE2) is expressed in human pancreatic β-cells and in the human pancreas microvasculature

Fignani

Licata

Brusco

et al. 2020

Preprint

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SummaryIncreasing evidence demonstrated that the expression of Angiotensin I-Converting Enzyme type 2 (ACE2), is a necessary step for SARS-CoV-2 infection permissiveness. In the light of the recent data highlighting an association between COVID-19 and diabetes, a detailed analysis aimed at evaluating ACE2 expression pattern distribution in human pancreas is still lacking. Here, we took advantage of INNODIA network EUnPOD biobank collection to thoroughly analyse ACE2, both at mRNA and protein level, in multiple human pancreatic tissues and using several methodologies. We showed that ACE2 is indeed present in human pancreatic islets, where is preferentially expressed by insulin producing β-cells. Of note, pro-inflammatory cytokines increased ACE2 expression in β-cells, thus putatively suggesting an enhancement of β-cells sensitivity to SARS-CoV-2 during inflammatory conditions. Taken together, our data indicate a potential link between SARS-CoV-2 infection and diabetes, through direct β-cell virus tropism.Highlights-Human pancreatic islets express SARS-CoV-2 receptor Angiotensin I-Converting Enzyme type 2 (ACE2)-In human pancreatic islets, ACE2 is preferentially expressed by β-cells-In human β-cells, ACE2 expression is increased upon inflammatory stress

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Section: Discussionmentioning

confidence: 88%

SARS-CoV-2 receptor Angiotensin I-Converting Enzyme type 2 (ACE2) is expressed in human pancreatic β-cells and in the human pancreas microvasculature

Fignani

Licata

Brusco

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Significantly, short-ACE2 is missing the aminoacidic residues reported as fundamental for virus binding; however, due to the lack of detailed data regarding its function we cannot exclude that the short-ACE2 may modulate SARS-CoV-2 susceptibility by interacting with long-ACE2 or additional membrane proteins which may mediate the binding to SARS-CoV-2 spike protein [e.g. ITGA5, as previously observed (61)]. Of interest, nasal epithelium, reported to represent the main reservoir of SARS-CoV-2 (62), showed higher levels of short-ACE2 vs. long-ACE2 (24).…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 Receptor Angiotensin I-Converting Enzyme Type 2 (ACE2) Is Expressed in Human Pancreatic β-Cells and in the Human Pancreas Microvasculature

et al. 2020

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“… 23 Similarly, integrin α5 or α5β1 dimer, known to mediate cell binding and entry of certain viruses, 24 binds to and is co-regulated with ACE2 in ventricular remodeling. 25 In the Vero E6 cell model, an α5β1 dimer inhibitor prevents SARS-CoV-2 infection and reduces binding of SARS-Cov-2 to ACE2. 26 Thus, α5βb1 integrin, likely through binding to α5, may also be an attachment factor or even a co-receptor for SARS-CoV-2 entry.…”

Section: Sars-cov-2 Viral Entry and Life Cyclementioning

confidence: 99%

COVID-19 and Cardiovascular Disease

Chung

Zidar

Bristow

et al. 2021

Circulation Research

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281

266

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A pandemic of historic impact, coronavirus disease 2019 (COVID-19) has potential consequences on the cardiovascular health of millions of people who survive infection worldwide. Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), the etiologic agent of COVID-19, can infect the heart, vascular tissues, and circulating cells through ACE2 (angiotensin-converting enzyme 2), the host cell receptor for the viral spike protein. Acute cardiac injury is a common extrapulmonary manifestation of COVID-19 with potential chronic consequences. This update provides a review of the clinical manifestations of cardiovascular involvement, potential direct SARS-CoV-2 and indirect immune response mechanisms impacting the cardiovascular system, and implications for the management of patients after recovery from acute COVID-19 infection.

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Dynamic Regulation of SARS-Cov-2 Binding and Cell Entry Mechanisms in Remodeled Human Ventricular Myocardium

Cited by 48 publications

References 55 publications

SARS-CoV-2 receptor Angiotensin I-Converting Enzyme type 2 (ACE2) is expressed in human pancreatic β-cells and in the human pancreas microvasculature

SARS-CoV-2 receptor Angiotensin I-Converting Enzyme type 2 (ACE2) is expressed in human pancreatic β-cells and in the human pancreas microvasculature

SARS-CoV-2 Receptor Angiotensin I-Converting Enzyme Type 2 (ACE2) Is Expressed in Human Pancreatic β-Cells and in the Human Pancreas Microvasculature

COVID-19 and Cardiovascular Disease

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