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10.1016/j.isci.2022.104685

http://scihub22266oqcxt.onion/10.1016/j.isci.2022.104685
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suck abstract from ncbi


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pmid35789750      iScience 2022 ; 25 (8): 104685
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  • Immunomodulatory LncRNA on antisense strand of ICAM-1 augments SARS-CoV-2 infection-associated airway mucoinflammatory phenotype #MMPMID35789750
  • Devadoss D; Acharya A; Manevski M; Houserova D; Cioffi MD; Pandey K; Nair M; Chapagain P; Mirsaeidi M; Borchert GM; Byrareddy SN; Chand HS
  • iScience 2022[Aug]; 25 (8): 104685 PMID35789750show ga
  • Noncoding RNAs are important regulators of mucoinflammatory response, but little is known about the contribution of airway long noncoding RNAs (lncRNAs) in COVID-19. RNA-seq analysis showed a more than 4-fold increased expression of IL-6, ICAM-1, CXCL-8, and SCGB1A1 inflammatory factors; MUC5AC and MUC5B mucins; and SPDEF, FOXA3, and FOXJ1 transcription factors in COVID-19 patient nasal samples compared with uninfected controls. A lncRNA on antisense strand to ICAM-1 or LASI was induced 2-fold in COVID-19 patients, and its expression was directly correlated with viral loads. A SARS-CoV-2-infected 3D-airway model largely recapitulated these clinical findings. RNA microscopy and molecular modeling indicated a possible interaction between viral RNA and LASI lncRNA. Notably, blocking LASI lncRNA reduced the SARS-CoV-2 replication and suppressed MUC5AC mucin levels and associated inflammation, and select LASI-dependent miRNAs (e.g., let-7b-5p and miR-200a-5p) were implicated. Thus, LASI lncRNA represents an essential facilitator of SARS-CoV-2 infection and associated airway mucoinflammatory response.
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