About: Downregulation of Paralemmin-3 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating Inflammatory Response and Inhibiting Formation of TLR4/MyD88 and TLR4/TRIF Complexes

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About: Downregulation of Paralemmin-3 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating Inflammatory Response and Inhibiting Formation of TLR4/MyD88 and TLR4/TRIF Complexes Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Downregulation of Paralemmin-3 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating Inflammatory Response and Inhibiting Formation of TLR4/MyD88 and TLR4/TRIF Complexes
Creator	Wang, Yi Tang, Lu Feng, Jian Chen, Xuxin Han, Zhihai Meng, Jiguang
source	PMC
abstract	Previous studies have demonstrated paralemmin-3 (PALM3) participates in Toll-like receptor (TLR) signaling. This study investigated the effect of PALM3 knockdown on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and its underlying mechanisms. We constructed a recombinant adenoviral vector containing short hairpin RNA for PALM3 to knockdown PALM3 expression. A transgene-free adenoviral vector was used as a negative control. The ALI rat model was established by LPS peritoneal injection at 48-h post-transfection. Results showed that downregulation of PALM3 improved the survival rate, attenuated lung pathological changes, alleviated pulmonary edema, lung vascular leakage and neutrophil infiltration, inhibited the production of proinflammatory cytokines and activation of nuclear factor κB and interferon β regulatory factor 3, and promoted the secretion of anti-inflammatory cytokine interleukin-10 and expression of suppressor of cytokine signaling-3 in the ALI rat model. However, PALM3 knockdown had no effect on TLR4, myeloid differentiation factor 88 (MyD88), and Toll-interleukin-1 receptor domain-containing adaptor inducing interferon β (TRIF) expression. Moreover, PALM3 knockdown reduced the interaction of TLR4 with MyD88 or TRIF induced by LPS in rat lungs. Therefore, the downregulation of PALM3 protected rats from LPS-induced ALI and its mechanisms were partially associated with the modulation of inflammatory responses and inhibition of TLR4/MyD88 and TLR4/TRIF complex formation.
has issue date	2017-08-12(xsd:dateTime)
bibo:doi	10.1007/s10753-017-0639-9
bibo:pmid	28801798
has license	no-cc
sha1sum (hex)	9f559c365b058f58fcb065cae456c3fe3aff67a7
schema:url	https://doi.org/10.1007/s10753-017-0639-9
resource representing a document's title	Downregulation of Paralemmin-3 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating Inflammatory Response and Inhibiting Formation of TLR4/MyD88 and TLR4/TRIF Complexes
has PubMed Central identifier	PMC7102376
has PubMed identifier	28801798
schema:publication	Inflammation
resource representing a document's body	covid:9f559c365b058f58fcb065cae456c3fe3aff67a7#body_text
is schema:about of	named entity 'interleukin' named entity 'ALI' named entity 'DOWNREGULATION' named entity 'DEMONSTRATED' named entity 'LUNG' named entity 'RESULTS' named entity 'UNDERLYING' named entity 'NEGATIVE CONTROL' named entity 'SUPPRESSOR OF CYTOKINE SIGNALING' named entity 'CONSTRUCTED' named entity 'TRIF' covid:arg/9f559c365b058f58fcb065cae456c3fe3aff67a7 named entity 'study' named entity 'However' named entity 'differentiation' named entity 'pathological' named entity 'reduced' named entity 'receptor' named entity 'participates' named entity 'expression' named entity 'negative control' named entity 'expression' named entity 'constructed' named entity 'proinflammatory cytokines' named entity 'inflammatory responses' named entity 'expression' named entity 'This' named entity 'modulation' named entity 'TLR4' named entity 'TRIF' named entity 'pulmonary edema' named entity 'suppressor of cytokine signaling' named entity 'negative control' named entity 'nuclear factor κB' named entity 'lung' named entity 'recombinant' named entity 'interleukin-10' named entity 'neutrophil' named entity 'myeloid' named entity 'acute lung injury' named entity 'antiinflammatory' named entity 'MyD88' named entity 'Downregulation' named entity 'LPS' named entity 'MyD88' named entity 'dendritic cells' named entity 'protein expression' named entity 'Laboratory Animal' named entity 'NF-κB' named entity 'interleukin' named entity 'homodimer' named entity 'Thermo Fisher Scientific' named entity 'adaptor proteins' named entity 'TLR4' named entity 'pathogenesis' named entity 'nucleus' named entity 'TLR4' named entity 'ALI' named entity 'IFN-β' named entity 'rat' named entity 'NF-κB' named entity 'downregulation' named entity 'NF-κB' named entity 'LPS' named entity 'p65' named entity 'anesthetized' named entity 'ALI' named entity 'polyclonal antibodies' named entity 'metastatic' named entity 'β-actin' named entity 'MPO' named entity 'lung injury' named entity 'antibody' named entity 'ALI' named entity 'TLR4' named entity 'translocation'

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