Department of Dermatovenereology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
J Cosmet Dermatol. 2021 Aug;20(8):2619-2626. doi: 10.1111/jocd.13898. Epub 2020 Dec 22.
Oral isotretinoin is the first-line treatment of severe nodular acne. However, patients presenting ineffective or poor effective to oral isotretinoin are still a clinical problem, and its molecular genetic mechanisms remain unclear.
To compare the transcriptome profiles of isotretinoin-effective and isotretinoin-ineffective severe acne vulgaris patients and analyze the potential physiological roles to better understand the mechanisms of isotretinoin efficacy differences.
PATIENTS/METHODS: Peripheral blood of 43 patients with severe acne was collected before treatment. After 8-week isotretinoin, patients presented effective and ineffective to isotretinoin treatment were selected and their pretreatment peripheral blood was analyzed. High-throughput sequencing was used to detect gene expression profiles. Gene Ontology and KEGG were used to perform functional annotation and pathway enrichment analysis.
Ten acne patients (3 male and 7 female, age 31 ± 9.2) presented effectiveness by oral isotretinoin and 10 acne patients (4 male and 6 female, age 28 ± 7.7) presented ineffectiveness were included. Comparison of gene profiles of isotretinoin-effective and isotretinoin-ineffective patients revealed 2779 differentially expressed genes: 2723 upregulated and 56 downregulated. Differentially expressed genes were enriched in RNA degradation pathway, autophagy pathway, protein ubiquitination pathway, protein processing in endoplasmic reticulum pathway, T-cell receptor signaling pathway, spliceosome pathway, mRNA surveillance pathway, cell cycle pathway, long-term potentiation pathway, and FoxO signaling pathway.
Transcriptome expression differences not only participated in the acne pathogenesis, but also influenced the isotretinoin therapeutic effects. These findings might provide some evidence for exploring individualized therapy for acne patients.
口服异维 A 酸是治疗严重结节性痤疮的一线药物。然而,对于口服异维 A 酸治疗无效或效果不佳的患者,仍然是一个临床问题,其分子遗传机制尚不清楚。
比较异维 A 酸治疗有效和无效的重度寻常性痤疮患者的转录组谱,并分析潜在的生理作用,以更好地了解异维 A 酸疗效差异的机制。
患者/方法:收集 43 例重度痤疮患者治疗前的外周血。经过 8 周异维 A 酸治疗后,选择对异维 A 酸治疗有效和无效的患者,并分析其治疗前外周血。采用高通量测序检测基因表达谱。使用基因本体论和 KEGG 进行功能注释和通路富集分析。
10 例(3 例男性,7 例女性,年龄 31±9.2)口服异维 A 酸有效,10 例(4 例男性,6 例女性,年龄 28±7.7)口服异维 A 酸无效的痤疮患者纳入研究。比较异维 A 酸有效和无效患者的基因谱,发现 2779 个差异表达基因:2723 个上调,56 个下调。差异表达基因富集于 RNA 降解途径、自噬途径、蛋白质泛素化途径、内质网蛋白加工途径、T 细胞受体信号通路、剪接体途径、mRNA 监测途径、细胞周期途径、长时程增强途径和 FoxO 信号通路。
转录组表达差异不仅参与了痤疮的发病机制,而且影响了异维 A 酸的治疗效果。这些发现可能为探索个体化治疗痤疮患者提供一些证据。