Title:Decoding the Transcriptional Response to Ischemic Stroke in Obese and Non-obese Mice Brain
Volume: 18
Issue: 2
Author(s): Jing Liang*, Ruiyao Hu*, Xin Wang, Xinjing Liu, Lulu Pei, Mengke Tian, Wenxian Sun, Luyang Zhang, Lan Ding, Yuying Wang, Yuming Xu and Bo Song
Affiliation:
- Department of Neurology, The First Affiliated Hospital of Zhengzhou University, No.1 Eastern Jianshe Road, Zhengzhou 450052, Henan,China
- Department of Neurology, The First Affiliated Hospital of Zhengzhou University, No.1 Eastern Jianshe Road, Zhengzhou 450052, Henan,China
Keywords:
Stroke, obesity, inflammation, NOD-like receptor, monocytes, KEGG.
Abstract:
Background: Ischemic Stroke (IS) is a serious cerebrovascular disease, which leads to irreversible
damage or death of brain cells. Effective control of stroke risk factors can effectively reduce
the incidence of IS. However, there was an “obesity paradox” about the relationship between
obesity and the prognosis of IS, in which obesity would not bring worse outcomes than non-obese
IS patients.
Objective: Herein, we aimed to investigate the transcriptional response to IS in obese and nonobese
mice brain via RNA-Seq technology. The datasets of obese and non-obese mice with/without
IS were obtained from the Gene Expression Omnibus (GEO) database.
Methods: Differentially expressed genes (DEGs) between Control and Obesity (DEGsObesity) and
between Obesity and Obese-Stroke (DEGsObese-Stroke) were identified. Gene Ontology (GO),
Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and Protein-Protein Interaction
(PPI) network analysis were performed to predict the function of DEGs. 28 and 109
DEGs were screened in DEGsObesity and DEGsObese-Stroke, respectively.
Results: Significantly, in the top 10 key-genes of DEGsObese-Stroke (Tnf, Lgals3, Serpinb2,
Ly6c2, Chil3, Clec4e, Mmp3, Mefv, Spn, Tlr8), Tnf and Mefv were involved in the NOD-like receptor
signaling pathway, which was consistent with KEGG pathway enrichment results. And Chil3,
as a mononuclear cell marker, was significantly elevated in Obese-Stroke compared with Stroke,
suggesting mononuclear cell, rather than other peripheral immune cells, infiltrated into the brain of
Obese-stroke.
Conclusion: Hence, we concluded that obesity could affect the brain microenvironment at the transcriptome
level and Stroke after obesity could lead to more changes in NOD-like receptor signaling
pathway and monocyte infiltration, compared with non-obese Stroke.
