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pmid:39738531

Bioinformatics Identification of angiogenesis-related biomarkers and therapeutic targets in cerebral ischemia-reperfusion.

Yong-Hong Wu · Jing Sun · Jun-Hua Huang · Xiao-Yun Lu

Scientific reports · 2024 doi:10.1038/s41598-024-83783-9

Paper

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Data

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partial

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Bioinformatics Identification of angiogenesis-related biomarkers and therapeutic targets in cerebral ischemia-reperfusion.
doi
10.1038/s41598-024-83783-9
pmid
39738531
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Yong-Hong Wu
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Jing Sun
[2]
Jun-Hua Huang
[3]
Xiao-Yun Lu
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Scientific reports
year
2024
abstract
Promoting vascular endothelial cell regeneration can enhance recovery from cerebral ischemia reperfusion injury (CIRI), but there is a lack of bioinformatic studies on angiogenesis-related biomarkers in CIRI. In this study, we utilized the GSE97537 and GSE61616 datasets from GEO to identify 181 angiogenesis-related genes (ARGs) and analyzed differentially expressed genes (DEGs) between CIRI and control groups. We converted ARGs to 169 rat homologues and intersected them with DEGs to find DE-ARGs. RF and XGBoost models were employed to identify five biomarkers (Stat3, Hmox1, Egfr, Col18a1, Ptgs2) and conducted GSEA on these biomarkers, revealing their enrichment in pathways such as ECM-receptor interaction and hematopoietic cell lineage. We also analyzed the immune microenvironment, finding significant differences in 21 immune cells between CIRI and control groups. Furthermore, we constructed lncRNA-miRNA-mRNA networks and drug-gene networks. Finally, biomarker expression was compared between the CIRI and control groups by qRT-PCR in tissue and blood samples. Overall, our bioinformatic exploration of angiogenesis-related biomarkers in CIRI provides new insights for the diagnosis and treatment of CIRI.
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First, random forest (RF) and extreme gradient boosting (XGBoost) analyses were performed on DE-ARGs to acquire corresponding genes respectively.
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First, random forest (RF) and extreme gradient boosting (XGBoost) analyses were performed on DE-ARGs to acquire corresponding genes respectively.
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Data Availability: The original data presented in the study are openly available in [Genecards database and MSigDB] at [https://www.ncbi.nlm.nih.gov/gds, https://www.gsea-msigdb.org/gsea/msigdb/index.jsp].
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Data Availability: The original data presented in the study are openly available in [Genecards database and MSigDB] at [https://www.ncbi.nlm.nih.gov/gds, https://www.gsea-msigdb.org/gsea/msigdb/index.jsp].
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Random forest and XGBoost analyses of differentially expressed angiogenesis-related genes identified Stat3, Hmox1, Egfr, Col18a1 and Ptgs2 as five angiogenesis-related biomarkers for cerebral ischemia reperfusion injury.
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sections[4] "Stat3, Hmox1, Egfr, Col18a1 and Ptgs2 were identified as biomarkers" paragraph 2
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Five biomarkers namely Stat3, Hmox1, Egfr, Col18a1 and Ptgs2 were derived after taking the intersection of genes obtained by RF and XGBoost (Fig. 2c), and they were all differentially expressed between CIRI and control samples in the two datasets, in which Ptgs2 expressed an opposite trend in the two datasets (Fig. 2d and e).
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Random forest and XGBoost analyses of differentially expressed angiogenesis-related genes identified Stat3, Hmox1, Egfr, Col18a1 and Ptgs2 as five angiogenesis-related biomarkers for cerebral ischemia reperfusion injury.
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Data Availability: The original data presented in the study are openly available in [Genecards database and MSigDB] at [https://www.ncbi.nlm.nih.gov/gds, https://www.gsea-msigdb.org/gsea/msigdb/index.jsp].
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and control groups. We converted ARGs to 169 rat homologues and intersected them with DEGs to
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d and tissue samples The SPF healthy male SD rats were obtained from Beijing Vital River Laboratory
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and water. Rats weighed 250–280 g when used. Rats were anaesthetized with isoflurane (Ruiwode, Shen
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First, random forest (RF) and extreme gradient boosting (XGBoost) analyses were performed on DE-ARGs to acquire corresponding genes respectively.
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In this study, we utilized the GSE97537 and GSE61616 datasets from GEO to identify 181 angiogenesis-related genes (ARGs) and analyzed differentially expressed genes (DEGs) between CIRI and control groups. We converted ARGs to 169 rat homologues and intersected them with DEGs to find DE-ARGs. RF and XGBoost models were employed to identify five biomarkers (Stat3, Hmox1, Egfr, Col18a1, Ptgs2) and conducted GSEA on these biomarkers, revealing their enrichment in pathways such as ECM-receptor interaction and hematopoietic cell lineage. We also analyzed the immune microenvironment, finding significant differences in 21 immune cells between CIRI and control groups. Furthermore, we constructed lncRNA-miRNA-mRNA networks and drug-gene networks. Finally, biomarker expression was compared between the CIRI and control groups by qRT-PCR in tissue and blood samples. 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