Purpose: The incidence of nonsuicidal self-injury (NSSI) behavior among adolescents increases year by year. Patients with a history of both depression and NSSI behaviors tend to have greater risk of suicide. At present, the mechanism of adolescent depressive disorder patients with NSSI behaviors is not clear, epigenetic mechanism may be involved. Proopiomelanocortin (POMC) gene may be associated with depressive disorder. The purpose of this study was to investigate DNA methylation of POMC gene promoter region of adolescent depressive disorder patients with NSSI behaviors.
Methods: Bisulfite Sequencing PCR (BSP) was used to test the methylation level of POMC promoter of 15 adolescent depressive disorder patients with NSSI behaviors and 15 healthy controls (HC). Self-made questionnaires were used to collect clinical data of the case group and control group. Hamilton depression scale-24 (HAMD-24), Hamilton anxiety scale (HAMA), Symptom Checklist-90 (SCL-90) were used to evaluate the characteristics and severity of depressive, anxiety and psychotic symptoms. Adolescent self-injury questionnaire was used to assess NSSI behaviors and its severity.
Results: BSP analysis found that the POMC methylation level of cytosine-guanine dinucleotide 1 (CpG1) site was higher in the case group than that of HC (P< 0.05). The significance in POMC methylation at CpG1 between case group and HC was gender-independent, and CpG1 methylation level was higher in both male (P< 0.05) and female (P< 0.05) patients than that in HC. The CpG1 methylation level had a little correlation trends with family history of psychosis (P=0.05). We also found that POMC methylation level at CpG17 in female patients was significantly higher than that of the female HC (P< 0.05).
Conclusion: There was abnormal methylation in the POMC promoter region of adolescent depressive disorder patients with NSSI behaviors, the methylation of CpG1 may act as epigenetic markers for those adolescents.

Keywords: adolescent, depressive disorder, POMC, methylation, nonsuicidal self-injury behavior

Erratum for this paper has been published


中文翻译：

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具有非自杀性自伤行为的青少年抑郁症患者 POMC 基因启动子区域的表观遗传改变

目的：青少年非自杀性自伤（NSSI）行为的发生率逐年增加。有抑郁症和 NSSI 行为史的患者往往有更大的自杀风险。目前，青少年抑郁症患者出现NSSI行为的机制尚不明确，可能涉及表观遗传机制。阿黑皮质素原 ( POMC ) 基因可能与抑郁症有关。本研究的目的是调查具有 NSSI 行为的青少年抑郁症患者POMC基因启动子区域的 DNA 甲基化情况。
方法：采用亚硫酸氢盐测序PCR（BSP）检测POMC甲基化水平15 名具有 NSSI 行为的青少年抑郁症患者和 15 名健康对照者 (HC) 的发起人。采用自制问卷收集病例组和对照组的临床资料。汉密尔顿抑郁量表24（HAMD-24）、汉密尔顿焦虑量表（HAMA）、症状检查表90（SCL-90）用于评估抑郁、焦虑和精神病症状的特征和严重程度。青少年自伤问卷用于评估 NSSI 行为及其严重程度。
结果： BSP分析发现病例组胞嘧啶-鸟嘌呤二核苷酸1（CpG1）位点POMC甲基化水平高于HC组（P <0.05）。POMC的意义病例组和HC之间CpG1甲基化水平与性别无关，男性（P < 0.05）和女性（P < 0.05）患者CpG1甲基化水平均高于HC。CpG1甲基化水平与精神病家族史有一定的相关性（P =0.05）。我们还发现女性患者CpG17的POMC甲基化水平显着高于女性HC（P < 0.05）。
结论：有NSSI行为的青少年抑郁症患者的POMC启动子区存在异常甲基化，CpG1的甲基化可能作为这些青少年的表观遗传标志物。

关键词：青少年，抑郁症，POMC，甲基化，非自杀性自伤行为

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