Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    Nicotine Changes Airway Epithelial Phenotype and May Increase the SARS-COV2 Infection MESHD Severity

    Authors: Leonardo Lupacchini; Fabrizio Maggi; Carlo Tomino; Chiara De Dominicis; Cristiana Mollinari; Massimo Fini; Stefano Bonassi; Daniela Merlo; Patrizia Russo

    id:10.20944/preprints202012.0467.v1 Date: 2020-12-18 Source:

    (1) Background: Nicotine is implicated in the SARS-COV-2 infection MESHD through activation of the α7- nAChR HGNC and over-expression of ACE2 HGNC. Our objective is to clarify the role of nicotine in SARS-CoV-2 infection MESHD exploring its molecular and cellular activity. (2) Methods: HBEpC or si-mRNA-α7-HBEpC were treated for 1, 48 h or continuously with 10-7 M Nicotine, a concentration mimicking human exposure to a cigarette. Cell viability and proliferation were evaluated by trypan blue dye exclusion and cell counting, migration by cell migration assay, senescence by SA-beta-Gal activity, and anchorage-independent growth by cloning in soft agar. Expression of Ki67, p53 HGNC/phospho- p53 HGNC, VEGF HGNC, EGFR HGNC/pEGFR, phospho-p38, intracellular Ca+2, ATP and EMT HGNC were evaluated by ELISA and/or western blotting. (3) Results: Nicotine induced through α7- nAChR HGNC (i) increase in cell viability (ii) cell proliferation; (iii) Ki67 over-expression, (iv) phospho-p38 up-regulation (v) EGFR HGNC/pEGFR over-expression; (vi) increase in basal Ca+2 concentration, (vii) reduction of ATP production; (viii) decreased level of p53 HGNC/phospho- p53 HGNC, (ix) delayed senescence, (x) VEGF increase, (xi) EMT and consequent (xii) enhanced migration, and (xiii) ability to grow independently of the substrate. (4) Conclusions: Based on our results and on evidence showing that Nicotine potentiates viral infection it is likely that Nicotine is involved in SARS-CoV-2 infection MESHD and severity

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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