About: miRNA-200c-3p is crucial in acute respiratory distress syndrome

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About: miRNA-200c-3p is crucial in acute respiratory distress syndrome Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	miRNA-200c-3p is crucial in acute respiratory distress syndrome
Creator	Zhao, Yan Xu, Jun Huang, Fengming Jiang, Chengyu Zhang, Cong Lu, Huijun Yu, Xuezhong Zhu, Huadong Li, Xiao Du, Jianchao Jin, Ningyi Liu, Qiang Tian, Mingyao Li, Chang Chang, Jiahui Li, Xiaoyun Shang, Daozhen Xu, Jiantao
Source	Medline; PMC
abstract	Influenza infection and pneumonia are known to cause much of their mortality by inducing acute respiratory distress syndrome (ARDS), which is the most severe form of acute lung injury (ALI). Angiotensin-converting enzyme 2 (ACE2), which is a negative regulator of angiotensin II in the renin–angiotensin system, has been reported to have a crucial role in ALI. Downregulation of ACE2 is always associated with the ALI or ARDS induced by avian influenza virus, severe acute respiratory syndrome-coronavirus, respiratory syncytial virus and sepsis. However, the molecular mechanism of the decreased expression of ACE2 in ALI is unclear. Here we show that avian influenza virus H5N1 induced the upregulation of miR-200c-3p, which was then demonstrated to target the 3′-untranslated region of ACE2. Then, we found that nonstructural protein 1 and viral RNA of H5N1 contributed to the induction of miR-200c-3p during viral infection. Additionally, the synthetic analog of viral double-stranded RNA (poly (I:C)), bacterial lipopolysaccharide and lipoteichoic acid can all markedly increase the expression of miR-200c-3p in a nuclear factor-κB-dependent manner. Furthermore, markedly elevated plasma levels of miR-200c-3p were observed in severe pneumonia patients. The inhibition of miR-200c-3p ameliorated the ALI induced by H5N1 virus infection in vivo, indicating a potential therapeutic target. Therefore, we identify a shared mechanism of viral and bacterial lung infection-induced ALI/ARDS via nuclear factor-κB-dependent upregulation of miR-200c-3p to reduce ACE2 levels, which leads increased angiotensin II levels and subsequently causes lung injury.
has issue date	2017-06-27(xsd:dateTime)
bibo:doi	10.1038/celldisc.2017.21
bibo:pmid	28690868
has license	cc-by
sha1sum (hex)	0b530925f860fe1a3191519482c19e8240834caf
schema:url	https://doi.org/10.1038/celldisc.2017.21
resource representing a document's title	miRNA-200c-3p is crucial in acute respiratory distress syndrome
has PubMed Central identifier	PMC5485385
has PubMed identifier	28690868
schema:publication	Cell Discov
resource representing a document's body	covid:0b530925f860fe1a3191519482c19e8240834caf#body_text
is schema:about of	named entity 'induced' named entity 'virus' named entity 'infection' named entity 'ALI' named entity 'viral' named entity 'severe' named entity 'acute lung injury' named entity 'infection' named entity '200c' covid:arg/0b530925f860fe1a3191519482c19e8240834caf named entity 'ACE2' named entity 'target' named entity 'Downregulation' named entity 'sepsis' named entity 'respiratory' named entity 'Here' named entity 'H5N1' named entity 'demonstrated' named entity 'vivo' named entity 'respiratory syncytial virus' named entity 'severe' named entity '3′-untranslated region' named entity 'renin-angiotensin system' named entity 'avian influenza' named entity 'upregulation' named entity 'inhibition' named entity '200c' named entity 'angiotensin II' named entity '3′-untranslated region' named entity 'ACE2' named entity 'respiratory syncytial virus' named entity 'ALI' named entity 'pneumonia' named entity 'ARDS' named entity 'lung infection' named entity 'severe pneumonia' named entity 'miR-200c' named entity 'therapeutic target' named entity 'ACE2' named entity 'ALI' named entity 'Downregulation' named entity 'ACE2' named entity 'ARDS' named entity 'ACE2' named entity 'lung tissue' named entity 'miR-200c' named entity 'pathogens' named entity 'intratracheal instillation' named entity 'cell proliferation' named entity 'qRT-PCR' named entity 'H5N1' named entity 'LPS' named entity 'ACE2' named entity 'ACE2' named entity 'plasma levels' named entity 'miR' named entity 'receptor' named entity 'influenza virus' named entity 'Toll-like receptor' named entity 'Invitrogen' named entity 'ARDS' named entity 'vector' named entity 'H5N1' named entity 'streptomycin'

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