دورية أكاديمية
أعرض في EDS

Inhibition of SARS-CoV-2 infection in human iPSC-derived cardiomyocytes by targeting the Sigma-1 receptor disrupts cytoarchitecture and beating.

التفاصيل البيبلوغرافية
العنوان: Inhibition of SARS-CoV-2 infection in human iPSC-derived cardiomyocytes by targeting the Sigma-1 receptor disrupts cytoarchitecture and beating.
المؤلفون: Salerno JA; Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Torquato T; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Temerozo JR; National Institute for Science and Technology on Neuroimmunomodulation (INCT/NIM), Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil.; Laboratory on Thymus Research, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Goto-Silva L; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Karmirian K; Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Mendes MA; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Sacramento CQ; Immunopharmacology Laboratory, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil.; National Institute for Science and Technology on Innovation in Diseases of Neglected Populations (INCT/IDPN), Center for Technological Development in Health (CDTS), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Fintelman-Rodrigues N; Immunopharmacology Laboratory, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil.; National Institute for Science and Technology on Innovation in Diseases of Neglected Populations (INCT/IDPN), Center for Technological Development in Health (CDTS), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Souza LRQ; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Ornelas IM; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Veríssimo CP; Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil., Aragão LGHS; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Vitória G; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Pedrosa CSG; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., da Silva Gomes Dias S; Immunopharmacology Laboratory, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Cardoso Soares V; Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.; Immunopharmacology Laboratory, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Puig-Pijuan T; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil.; Carlos Chagas Filho Institute of Biophysics (IBCCF), Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil., Salazar V; Department of Systems and Computer Engineering, COPPE, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil., Dariolli R; Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States of America.; PluriCell Biotech, São Paulo, Brazil., Biagi D; PluriCell Biotech, São Paulo, Brazil., Furtado DR; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Barreto Chiarini L; Carlos Chagas Filho Institute of Biophysics (IBCCF), Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil., Borges HL; Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil., Bozza PT; Immunopharmacology Laboratory, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Zaluar P Guimarães M; Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil., Souza TML; Immunopharmacology Laboratory, Oswaldo Cruz Institute (IOC), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil.; National Institute for Science and Technology on Innovation in Diseases of Neglected Populations (INCT/IDPN), Center for Technological Development in Health (CDTS), Oswaldo Cruz Foundation (Fiocruz), Rio de Janeiro, Brazil., Rehen SK; D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil.; Department of Genetics, Institute of Biology, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
المصدر: PeerJ [PeerJ] 2021 Dec 20; Vol. 9, pp. e12595. Date of Electronic Publication: 2021 Dec 20 (Print Publication: 2021).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: PeerJ Inc Country of Publication: United States NLM ID: 101603425 Publication Model: eCollection Cited Medium: Print ISSN: 2167-8359 (Print) Linking ISSN: 21678359 NLM ISO Abbreviation: PeerJ Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Corte Madera, CA : PeerJ Inc.
مستخلص: SARS-CoV-2 infects cardiac cells and causes heart dysfunction. Conditions such as myocarditis and arrhythmia have been reported in COVID-19 patients. The Sigma-1 receptor (S1R) is a ubiquitously expressed chaperone that plays a central role in cardiomyocyte function. S1R has been proposed as a therapeutic target because it may affect SARS-CoV-2 replication; however, the impact of the inhibition of S1R in human cardiomyocytes remains to be described. In this study, we investigated the consequences of S1R inhibition in iPSC-derived human cardiomyocytes (hiPSC-CM). SARS-CoV-2 infection in hiPSC-CM was productive and reduced cell survival. S1R inhibition decreased both the number of infected cells and viral particles after 48 hours. S1R inhibition also prevented the release of pro-inflammatory cytokines and cell death. Although the S1R antagonist NE-100 triggered those protective effects, it compromised cytoskeleton integrity by downregulating the expression of structural-related genes and reducing beating frequency. Our findings suggest that the detrimental effects of S1R inhibition in human cardiomyocytes' integrity may abrogate its therapeutic potential against COVID and should be carefully considered.
Competing Interests: Rafael Dariolli and Diogo Biagi were employed by PluriCell Biotech. The remaining authors declare that they have no competing interests.
(©2021 Salerno et al.)
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فهرسة مساهمة: Keywords: Cardiomyocyte; IPSC; SARS-CoV-2; Sigma-1 Receptor
تواريخ الأحداث: Date Created: 20220117 Latest Revision: 20231108
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC8697769
DOI: 10.7717/peerj.12595
PMID: 35036128
قاعدة البيانات: MEDLINE
الوصف
تدمد:2167-8359
DOI:10.7717/peerj.12595