Expression of SARS-CoV-2 entry factors in lung epithelial stem cells and its potential implications for COVID-19

Valyaeva, Anna A.; Zharikova, Anastasia A.; Kasianov, Artem S.; Vassetzky, Yegor S.; Sheval, Eugene V.

doi:10.1038/s41598-020-74598-5

Cited by 38 publications

(49 citation statements)

References 50 publications

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“…Moreover, we detected a pronounced ACE2 upregulation in wild type mouse embryonic stem cells ( Figure 3A – 3C , see dd0). Similarly, Valyaeva et al (2020) [ 18 ] documented that adult stem cells can be infected by SARS-CoV-2, which could affect the self-renewal of these cells and their potential to differentiate into various cell types, the main prerequisite of tissue regeneration.…”

Section: Discussionmentioning

confidence: 99%

Cell differentiation and aging accompanied by depletion of the ACE2 protein

Bártová

Legartová

Krejčí

et al. 2020

Aging

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Section: Discussionmentioning

confidence: 99%

Cell differentiation and aging accompanied by depletion of the ACE2 protein

Bártová

Legartová

Krejčí

et al. 2020

Aging

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“…It should also be considered that lungs from recovered COVID-19-infected patients may not regain full structural and functional integrity in severe cases since the repair or rebuilding capacity primarily depends on existing stem/progenitor populations. Early reports indicate lung epithelial stem cells may express SARS-CoV-2 entry factors higher than previously thought [ 25 , 26 ]. Lung contains functionally distinct candidate stem/progenitor cells such as basal cells [ 27 ], club cells [ 28 , 29 ], bronchoalveolar stem cells (BASCs) [ 30 ], and type II pneumocytes [ 31 ] involved in repair and regeneration of injured lungs.…”

Section: Tissue-specific Stem Cells and Covid Pathogenesismentioning

confidence: 99%

Experimental Models to Study COVID-19 Effect in Stem Cells

Chugh

Bhanja

Norris

et al. 2021

Cells

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The new strain of coronavirus (severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2)) emerged in 2019 and hence is often referred to as coronavirus disease 2019 (COVID-19). This disease causes hypoxic respiratory failure and acute respiratory distress syndrome (ARDS), and is considered as the cause of a global pandemic. Very limited reports in addition to ex vivo model systems are available to understand the mechanism of action of this virus, which can be used for testing of any drug efficacy against virus infectivity. COVID-19 induces tissue stem cell loss, resulting inhibition of epithelial repair followed by inflammatory fibrotic consequences. Development of clinically relevant models is important to examine the impact of the COVID-19 virus in tissue stem cells among different organs. In this review, we discuss ex vivo experimental models available to study the effect of COVID-19 on tissue stem cells.

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“…In line with SARS-CoV-2 infection influence on HSC biology, other stem cells, such as neural and lung epithelial stem cells, express ACE2 and may also be infected. In this regard, interference of COVID-19 has been proposed to contribute to neurological and respiratory symptoms’ manifestation [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

P2Y14 Receptor as a Target for Neutrophilia Attenuation in Severe COVID-19 Cases: From Hematopoietic Stem Cell Recruitment and Chemotaxis to Thrombo‐inflammation

Petiz

Glaser

Scharfstein

et al. 2021

Stem Cell Rev and Rep

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Graphical Abstract The global SARS-CoV-2 pandemic starting in 2019 has already reached more than 2.3 million deaths. Despite the scientific community’s efforts to investigate the COVID-19 disease, a drug for effectively treating or curing patients yet needs to be discovered. Hematopoietic stem cells (HSC) differentiating into immune cells for defense express COVID-19 entry receptors, and COVID-19 infection hinders their differentiation. The importance of purinergic signaling in HSC differentiation and innate immunity has been recognized. The metabotropic P2Y14 receptor subtype, activated by UDP-glucose, controls HSC differentiation and mobilization. Thereon, the exacerbated activation of blood immune cells amplifies the inflammatory state observed in COVID-19 patients, specially through the continuous release of reactive oxygen species and extracellular neutrophil traps (NETs). Further, the P2Y14 subtype, robustly inhibits the infiltration of neutrophils into various epithelial tissues, including lungs and kidneys. Here we discuss findings suggesting that antagonism of the P2Y14 receptor could prevent the progression of COVID-19-induced systemic inflammation, which often leads to severe illness and death cases. Considering the modulation of neutrophil recruitment of extreme relevance for respiratory distress and lung failure prevention, we propose that P2Y14 receptor inhibition by its selective antagonist PPTN could limit neutrophil recruitment and NETosis, hence limiting excessive formation of oxygen reactive species and proteolytic activation of the kallikrein-kinin system and subsequent bradykinin storm in the alveolar septa of COVID-19 patients.

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Expression of SARS-CoV-2 entry factors in lung epithelial stem cells and its potential implications for COVID-19

Cited by 38 publications

References 50 publications

Cell differentiation and aging accompanied by depletion of the ACE2 protein

Cell differentiation and aging accompanied by depletion of the ACE2 protein

Experimental Models to Study COVID-19 Effect in Stem Cells

P2Y14 Receptor as a Target for Neutrophilia Attenuation in Severe COVID-19 Cases: From Hematopoietic Stem Cell Recruitment and Chemotaxis to Thrombo‐inflammation

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