Bioinformatic analysis identifies GPR91 as a potential key gene in brain injury after deep hypothermic low flow

Explore the transcription change of brain ischemia and reperfusion injury after deep hypothermic low flow. The data from PRJNA739516 and GSE104036 were obtained for the differentially expressed genes identification, functional enrichment analysis, gene set enrichment analysis, protein-protein intera...

Full description

Saved in:
Bibliographic Details
Published inHeliyon Vol. 9; no. 5; p. e15286
Main Authors Puwei, Song, Jiali, Xu, Zhuoga, Deqin, Kede, Wu, Patel, Nishant, Jia, An, Jirong, Qi, Xuming, Mo
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.05.2023
Elsevier
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Explore the transcription change of brain ischemia and reperfusion injury after deep hypothermic low flow. The data from PRJNA739516 and GSE104036 were obtained for the differentially expressed genes identification, functional enrichment analysis, gene set enrichment analysis, protein-protein interaction construction and hub gene identification. Oxygen and glucose deprivation model was set to validate the hub gene and explore the detailed brain injury mechanism. Interleukin, immunological response, NF-κB signaling pathway, G protein-coupled receptor signaling pathway and NLRP inflammatory are functional pathway were enriched in differentially expressed genes analysis. Sucnr1, Casr, Cxcr4, C5ar1, Tas2r41, Tas2r60 and Hcar2 were identified and verified in the OGD model. Knocking down GPR91 reduces the inflammatory response after OGD and GPR91 may be involved in the inflammatory pre-reaction through the synergistic activation of NF-κB, NLRP3, and IL-1β respectively. Our study found that Interleukin, immunological response, NF-κB signaling pathway, G protein-coupled receptor signaling pathway and NLRP inflammatory are all associated with brain ischemia and reperfusion injury after deep hypothermic low flow and GPR91 can activate NF-κB/NLRP3 pathway and trigger the release of IL-1β in this progress.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Mo Xuming and Qi Jirong contributed equal efforts and should be listed as co-corresponding authors.
Song Puwei, Xu Jiali and Deqin Zhuoga contributed equal efforts and should be listed as co-first authors.
ISSN:2405-8440
2405-8440
DOI:10.1016/j.heliyon.2023.e15286