Background: The occurrence of keloids tends to show family clusters and more severe symptoms in patients with a family history of the condition, but their pathological mechanisms remain unclear. In this study, we aimed to investigate the differences in genetic susceptibility between keloid patients with a family history of keloids and sporadic patients with sporadic keloids and explore potential therapeutic targets of keloids at the molecular level.
Methods: High-throughput sequencing data were obtained from normal skin tissue of patients with a family history of keloids (FN group) and normal skin tissue from sporadic patients (N group). Bioinformatics analysis was employed to identify hub genes. Promising hub genes were identified using RT-qPCR, immunohistochemistry and immunofluorescence assays, and Western blotting. GO and KEGG pathway enrichment analysis was performed to determine the main functions between the two groups.
Results: Patients with a family history of keloids had more severe clinical symptoms (Ρ = -0.749, P < 0.001). The expression of IL-4 and CCR7 was significantly different between patients with a family history of keloids and those with sporadic keloids. The high expression of IL-4 and the low expression of CCR7 in the FN group may be of key importance in explaining why keloids run in families (P < 0.05).
Conclusion: Having a family history of keloids is a risk factor for increased severity of keloids. IL-4 and CCR7 play an important role in the development of keloids in patients with a family history of the condition and may represent new targets for the treatment of keloids.
Keywords: Keloids; bioinformatics; differentially expressed genes; family history.
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