Format

Send to

Choose Destination
Am J Transl Res. 2018 Jul 15;10(7):2126-2136. eCollection 2018.

Bioinformatics-based analysis of the involvement of AC005550.3, RP11-415D17.3, and RP1-140K8.5 in homocysteine-induced vascular endothelial injury.

Author information

1
Geriatrics Department, Tongji Hospital Affiliated to Tongji University Medical School Shanghai 200065, China.

Abstract

This study aimed to explore the role of certain genes and long non-coding RNAs (lncRNAs) in homocysteine (HCY)-induced vascular endothelial injury. HUVECs were treated with HCY, then cell cycle and apoptosis were analyzed by flow cytometry. HUVECs were then sequenced and analyzed using bioinformatics, with a focus on differentially expressed genes/lncRNA (DEGs/DEL), protein-protein interaction (PPI), functional enrichment analyses, and lncRNA-target prediction. Although HCY did not affect the cell cycle, it significantly increased the number of apoptotic cells. In total, 382 DEGs and 147 DELs were identified; DEGs such as CD34, FGF2, and SERPINE1 were the hub nodes in the PPI network, in addition to being the targets of AC005550.3, RP11-415D17.3, and RP1-140K8.5, respectively. Functional enrichment analysis showed that the targets of downregulated AC005550.3 and RP11-415D17.3 were significantly enriched in blood vessel development and those of upregulated RP1-140K8.5 were enriched in fibrinolysis. RT-qPCR showed that the mRNA levels of AC005550.3, RP11-415D17.3, and RP1-140K8.5 were consistent with the results predicted by our bioinformatics analysis. In conclusion, downregulated AC005550.3 and RP11-415D17.3 targeting CD34 and FGF2 and upregulated RP1-140K8.5 targeting SERPINE1 may play an important role in HCY-induced vascular endothelial injury by regulating blood vessel development and fibrinolysis, respectively.

KEYWORDS:

Vascular endothelial injury; cardiovascular disease; homocysteine; long non-coding RNA; transcriptome sequence

PMID:
30093949
PMCID:
PMC6079138

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center