miR-24 Targets the Transmembrane Glycoprotein Neuropilin-1 in Human Brain Microvascular Endothelial Cells

Mone, Pasquale; Gambardella, Jessica; Wang, Xujun; Jankauskas, Stanislovas S.; Matarese, Alessandro; Santulli, Gaetano

doi:10.3390/ncrna7010009

Cited by 50 publications

(47 citation statements)

References 94 publications

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“…It was hypothesized that the respiratory breakdown in COVID-19 patients may be at least in part caused by SARS-CoV-2 infecting respiratory centers in the medulla oblongata and the pons [ 90 , 91 ]. It was also proposed that neuropilin-1 (NRP1), a transmembrane receptor expressed in the respiratory and olfactory epithelium as well as in the CNS endothelial cells, may serve as an alternative cell receptor and facilitate SARS-CoV2 entry into the brain [ 36 , 37 , 102 ].…”

Section: Ace2 and Organ Tropism Of Sars-cov2mentioning

confidence: 99%

Lock, Stock and Barrel: Role of Renin-Angiotensin-Aldosterone System in Coronavirus Disease 2019

Zanza

Tassi

Romenskaya

et al. 2021

Cells

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Since the end of 2019, the medical-scientific community has been facing a terrible pandemic caused by a new airborne viral agent known as SARS-CoV2. Already in the early stages of the pandemic, following the discovery that the virus uses the ACE2 cell receptor as a molecular target to infect the cells of our body, it was hypothesized that the renin-angiotensin-aldosterone system was involved in the pathogenesis of the disease. Since then, numerous studies have been published on the subject, but the exact role of the renin-angiotensin-aldosterone system in the pathogenesis of COVID-19 is still a matter of debate. RAAS represents an important protagonist in the pathogenesis of COVID-19, providing the virus with the receptor of entry into host cells and determining its organotropism. Furthermore, following infection, the virus is able to cause an increase in plasma ACE2 activity, compromising the normal function of the RAAS. This dysfunction could contribute to the establishment of the thrombo-inflammatory state characteristic of severe forms of COVID-19. Drugs targeting RAAS represent promising therapeutic options for COVID-19 sufferers.

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Section: Ace2 and Organ Tropism Of Sars-cov2mentioning

confidence: 99%

Lock, Stock and Barrel: Role of Renin-Angiotensin-Aldosterone System in Coronavirus Disease 2019

Zanza

Tassi

Romenskaya

et al. 2021

Cells

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“… 15 Additionally, other host factors enable and/or facilitate viral entry, such as transmembrane protease serine 2 (TMPRSS2), which acts on protein S priming; furin paired basic amino acid cleaving enzyme (FURIN), which activates protein substrates and pathogenic agents; and neuropilin-1 (NRP1), involved in angiogenesis and highly expressed on vascular cells and epithelia facing external environment, and which participates in tissue infiltration. 16 − 20 Although most research on virus entry focuses on ACE2, it is understandable that the availability of virus receptors and the interaction among cofactors help determine infectivity; in the case of SARS-CoV-2, cells with low ACE2 expression are also infected, which could be explained by the involvement of cofactors. 16 , 17 In addition, diverse genes have been reported to be upregulated in patients that develop severe COVID-19, possibly due to a direct correlation with the viral cycle in the human organism; these include ADAM metallopeptidase domain 10 (ADAM10), Toll-like receptor 3 (TLR3), histone acetyltransferase 1 (HAT1), histone deacetylase 2 (HDAC2), lysine demethylase 5B (KDM5B), sirtuin 1 (SIRT1), member renin-angiotensin system (RAS) oncogene family (RAB1A), and FURIN.…”

Section: Introductionmentioning

confidence: 99%

Airway and Alveoli Organoids as Valuable Research Tools in COVID-19

Oliveira

Síbio

Costa

et al. 2021

ACS Biomater. Sci. Eng.

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The coronavirus disease 2019 (COVID-19), caused by the novel coronavirus, SARS-CoV-2, affects tissues from different body systems but mostly the respiratory system, and the damage evoked in the lungs may occasionally result in severe respiratory complications and eventually lead to death. Studies of human respiratory infections have been limited by the scarcity of functional models that mimic in vivo physiology and pathophysiology. In the last decades, organoid models have emerged as potential research tools due to the possibility of reproducing in vivo tissue in culture. Despite being studied for over one year, there is still no effective treatment against COVID-19, and investigations using pulmonary tissue and possible therapeutics are still very limited. Thus, human lung organoids can provide robust support to simulate SARS-CoV-2 infection and replication and aid in a better understanding of their effects in human tissue. The present review describes methodological aspects of different protocols to develop airway and alveoli organoids, which have a promising perspective to further investigate COVID-19.

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“…We recently demonstrated that miR-24 is expressed in human brain endothelial cells (ECs) and targets Neuropilin-1 [ 4 ], a co-factor needed for SARS-CoV-2 internalization that has been linked to cerebrovascular (CBV) manifestations of COVID-19 [ 5 ]. Henceforth, we hypothesized an association between plasma levels of endothelial EV miR-24 and the onset of CBV events in patients hospitalized for COVID-19.…”

mentioning

confidence: 99%

“…A SARS-CoV-2 test (RT-qPCR) was performed in all subjects to confirm or rule out the COVID-19 diagnosis. EC-EVs were extracted from the plasma collected from these patients via serial centrifugation and CD31 + magnetic isolation [ 1 ], and EC-EVs miR-24 levels were quantified as described [ 1 , 4 , 6 ].…”

mentioning

confidence: 99%