About: XB130 deficiency enhances lipopolysaccharide-induced septic response and acute lung injury

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About: XB130 deficiency enhances lipopolysaccharide-induced septic response and acute lung injury Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	XB130 deficiency enhances lipopolysaccharide-induced septic response and acute lung injury
Creator	Tian, Feng Liu, Mingyao Bai, Xiaohui Cho, Hae-Ra Keshavjee, Shaf Adeyi, Oyedele Guan, Zhehong Toba, Hiroaki Tomankova, Tereza Wang, Yingchun
Source	PMC
abstract	XB130 is a novel oncoprotein that promotes cancer cell survival, proliferation and migration. Its physiological function in vivo is largely unknown. The objective of this study was to determine the role of XB130 in lipopolysaccharide (LPS)-induced septic responses and acute lung injury. LPS was intraperitoneally administrated to Xb130 knockout (KO) and wild type (WT) mice. There was a significant weight loss in KO mice at Day 2 and significantly higher disease scores during the 7 days of observation. The levels of tumor necrosis factor-alpha, monocyte chemoattractant protein-1, interleukin-6 and interleukin-10 in the serum were significantly higher in KO mice at Day 2. In KO mice there were a significantly higher lung injury score, higher wet/dry lung weight ratio, more apoptotic cells and less proliferative cells in the lung. Macrophage infiltration was significantly elevated in the lung of KO mice. There was significantly increased number of p-GSK-3β positive cells in KO mice, which were mainly neutrophils and macrophages. XB130 is expressed in alveolar type I and type II cells in the lung. The expression in these cells was significantly reduced after LPS challenge. XB130 deficiency delayed the recovery from systemic septic responses, and the presence of XB130 in the alveolar epithelial cells may provide protective mechanisms by reducing cell death and promoting cell proliferation, and reducing pulmonary permeability.
has issue date	2016-03-23(xsd:dateTime)
bibo:doi	10.18632/oncotarget.8326
bibo:pmid	27029000
has license	cc-by
sha1sum (hex)	50ad279de0a3f825b6280e07afc79439f59ecc3a
schema:url	https://doi.org/10.18632/oncotarget.8326
resource representing a document's title	XB130 deficiency enhances lipopolysaccharide-induced septic response and acute lung injury
has PubMed Central identifier	PMC5041914
has PubMed identifier	27029000
schema:publication	Oncotarget
resource representing a document's body	covid:50ad279de0a3f825b6280e07afc79439f59ecc3a#body_text
is schema:about of	named entity 'LPS' named entity 'presence' named entity 'Day' named entity 'interleukin' named entity 'DEFICIENCY' named entity 'SCORE' covid:arg/50ad279de0a3f825b6280e07afc79439f59ecc3a named entity 'EXPRESSION' named entity 'CELLS' named entity 'MICE' named entity 'RESPONSES' named entity 'IN VIVO' named entity 'MONOCYTE CHEMOATTRACTANT PROTEIN-1' named entity 'IS A' named entity 'WEIGHT RATIO' named entity 'THESE' named entity 'LIPOPOLYSACCHARIDE' named entity 'SCORES' named entity 'LUNG' named entity 'POSITIVE' named entity 'LPS' named entity 'HIGHER' named entity 'MACROPHAGES' named entity 'SIGNIFICANT' named entity 'DAY 2' named entity 'WET' named entity 'REDUCED' named entity 'INTERLEUKIN-6 ' named entity 'INDUCED' named entity 'CELL PROLIFERATION' named entity 'PULMONARY' named entity 'ITS' named entity 'NEUTROPHILS' named entity 'PROLIFERATIVE' named entity 'STUDY' named entity 'PRESENCE OF' named entity 'LUNG WEIGHT' named entity 'CELL SURVIVAL' named entity 'DISEASE' named entity 'CELL DEATH' named entity 'APOPTOTIC' named entity 'LARGELY' named entity 'MACROPHAGE INFILTRATION' named entity 'TUMOR NECROSIS FACTOR-ALPHA' named entity 'XB130' named entity 'DETERMINE' named entity 'ELEVATED' named entity 'PERMEABILITY' named entity 'CANCER CELL' named entity 'OBSERVATION' named entity 'SYSTEMIC' named entity 'SERUM' named entity 'TYPE II' named entity 'LUNG INJURY' named entity 'REDUCING' named entity 'ACUTE LUNG INJURY' named entity 'PHYSIOLOGICAL FUNCTION' named entity 'MIGRATION' named entity 'CHALLENGE' named entity 'KNOCKOUT' named entity 'UNKNOWN' named entity 'LEVELS' named entity 'PROLIFERATION' named entity 'DAYS' named entity 'OBJECTIVE' named entity 'RECOVERY' named entity 'TYPE I' named entity 'INTERLEUKIN-10 ' named entity 'NOVEL' named entity 'WAS A' named entity 'EXPRESSED' named entity 'ONCOPROTEIN'

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