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2018 ; 18
(1
): 31-40
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Identification of genes and pathways associated with multiple organ dysfunction
syndrome by microarray analysis
#MMPMID29749505
Gu C
; Qiao W
; Wang L
; Li M
; Song K
Mol Med Rep
2018[Jul]; 18
(1
): 31-40
PMID29749505
show ga
Multiple organ dysfunction syndrome (MODS) is characterized by the development of
progressive physiological dysfunction of ?2 organs or organ systems and is
responsible for the majority of the morbidity and mortality among patients in
intensive care units. The aim of the present study was to investigate the
potential genes and pathways associated with MODS. The microarray dataset
GSE60088 was downloaded from the Gene Expression Omnibus and used to identify
differentially expressed genes (DEGs) between organ tissues (lung, liver and
kidney) obtained from a murine model of MODS and healthy controls. The
interactions between DEGs in lungs, liver and kidneys were revealed by Kyoto
Encyclopedia of Genes and Genomes pathway enrichment analysis. Furthermore,
protein?protein interaction (PPI) data for DEGs were obtained from the Search
Tool for the Retrieval of Interacting Genes and a PPI network was constructed.
Additionally, DEGs that were common among the three organs were screened and
transcription factors that regulated them were predicted using the iRegulon
plugin. A total of 943, 267 and 227 DEGs were identified in lung, liver and
kidney samples, respectively, between mice with MODS and healthy controls. In
lung and liver samples, two pathways that were enriched with DEGs were identified
and were common between lung and liver samples, including 'cytokine?cytokine
receptor interaction' and 'Jnk?STAT signaling pathway', and examples of DEGs
associated with these pathways include C?X?C motif chemokine ligand (Cxcl)1 and
Cxcl10, and signal transducer and activator of transcription (Stat)1,
respectively. Furthermore, two common pathways were identified in liver and
kidney samples, which included 'MAPK signaling pathway' and 'p53 signaling
pathway', and DEGs associated with these pathways included growth arrest and DNA
damage?inducible ?. A total of 18 DEGs were common among lung, liver and kidney
tissues, including CCAAT/enhancer binding protein ? (Cebpb) and olfactomedin?like
1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was
regulated by Stat5A. These genes and pathways may serve roles in the progression
of MODS and may be considered to be potential therapy targets for MODS.