دورية أكاديمية

Increased mTOR Signaling and Impaired Autophagic Flux Are Hallmarks of SARS-CoV-2 Infection

التفاصيل البيبلوغرافية
العنوان: Increased mTOR Signaling and Impaired Autophagic Flux Are Hallmarks of SARS-CoV-2 Infection
المؤلفون: Érika Pereira Zambalde, Thomaz Luscher Dias, Grazielle Celeste Maktura, Mariene R. Amorim, Bianca Brenha, Luana Nunes Santos, Lucas Buscaratti, João Gabriel de Angeli Elston, Mariana Camargo Silva Mancini, Isadora Carolina Betim Pavan, Daniel A. Toledo-Teixeira, Karina Bispo-dos-Santos, Pierina L. Parise, Ana Paula Morelli, Luiz Guilherme Salvino da Silva, Ícaro Maia Santos de Castro, Tatiana D. Saccon, Marcelo A. Mori, Fabiana Granja, Helder I. Nakaya, Jose Luiz Proenca-Modena, Henrique Marques-Souza, Fernando Moreira Simabuco
المصدر: Current Issues in Molecular Biology, Vol 45, Iss 1, Pp 327-336 (2022)
بيانات النشر: MDPI AG, 2022.
سنة النشر: 2022
المجموعة: LCC:Biology (General)
مصطلحات موضوعية: COVID-19, single-cell analysis, autophagic flux, SARS-CoV-2, mTOR, Biology (General), QH301-705.5
الوصف: The COVID-19 (Coronavirus Disease 2019), caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), severely affects mainly individuals with pre-existing comorbidities. Here our aim was to correlate the mTOR (mammalian/mechanistic Target of Rapamycin) and autophagy pathways with the disease severity. Through western blotting and RNA analysis, we found increased mTOR signaling and suppression of genes related to autophagy, lysosome, and vesicle fusion in Vero E6 cells infected with SARS-CoV-2 as well as in transcriptomic data mining of bronchoalveolar epithelial cells from severe COVID-19 patients. Immunofluorescence co-localization assays also indicated that SARS-CoV-2 colocalizes within autophagosomes but not with a lysosomal marker. Our findings indicate that SARS-CoV-2 can benefit from compromised autophagic flux and inhibited exocytosis in individuals with chronic hyperactivation of mTOR signaling.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1467-3045
1467-3037
Relation: https://www.mdpi.com/1467-3045/45/1/23; https://doaj.org/toc/1467-3037; https://doaj.org/toc/1467-3045
DOI: 10.3390/cimb45010023
URL الوصول: https://doaj.org/article/100e2fe393e1485f9350e2393da3bc1e
رقم الأكسشن: edsdoj.100e2fe393e1485f9350e2393da3bc1e
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14673045
14673037
DOI:10.3390/cimb45010023