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载脂蛋白D和雄激素受体在腋臭中的表达及其分子机制。

Expression of apolipoprotein D and androgen receptor in axillary osmidrosis and its molecular mechanism.

作者信息

Chen Hui, Yang Guodong, Li Yingli, Li Xiaoli, Du Jie

机构信息

Deparment of Plastic Surgery and Burn, Tangdu, Hospital, The Fourth Military Medical University Xi'an 710038, China.

出版信息

Int J Clin Exp Med. 2013 Aug 1;6(7):497-503. Print 2013.

Abstract

OBJECTIVE

To investigate the expression of apolipoprotein D (ApoD) and androgen receptor (AR), two proteins related to E-3M2H secretion, in the apocrine sweat gland of patients with axillary osmidrosis (AO) and healthy subjects, and to explore the cause of abnormal ApoD expression in these patients.

METHODS

Samples were collected from healthy controls (n=4) and AO patients (n=10). Immunohistochemistry, real-time PCR and western blot assay were performed to measure the mRNA and protein expression of ApoD and AR. In vitro sweat gland cells were treated with androgen to explore the AR signals in regulation of ApoD expression and the role of JNK1 signaling pathway in the ApoD expression.

RESULTS

There was significant difference in the expression of ApoD and AR between AO patients and healthy controls. The ApoD expression in AO patients was 2-fold higher than that in healthy controls and the AR expression in AO patients was also markedly increased when compared with healthy controls. Moreover, the activation of JNK1 increased in AO patients. Androgen can increase the ApoD expression in healthy subjects accompanied bu JNK1 activation. Inhibition of JNK1 activation may reduce the ApoD expression in AO patients and the androgen induced ApopD expression.

CONCLUSION

The increase ApoD expression is closely related to the AR signaling pathway. JNK1 activation is a major cause of increased ApoD expression in AO patients and the androgen induced ApopD expression. To inhibit the JNK1 activation may suppress the endogenous ApoD expression in AO patients and the androgen induced ApopD expression.

摘要

目的

研究腋臭(AO)患者和健康受试者顶泌汗腺中与E-3M2H分泌相关的两种蛋白——载脂蛋白D(ApoD)和雄激素受体(AR)的表达情况,并探讨这些患者中ApoD表达异常的原因。

方法

从健康对照者(n = 4)和AO患者(n = 10)中采集样本。采用免疫组织化学、实时荧光定量PCR和蛋白质印迹法检测ApoD和AR的mRNA及蛋白表达。对体外培养的汗腺细胞用雄激素处理,以探究AR信号在调节ApoD表达中的作用以及JNK1信号通路在ApoD表达中的作用。

结果

AO患者与健康对照者之间ApoD和AR的表达存在显著差异。AO患者的ApoD表达比健康对照者高2倍,且与健康对照者相比,AO患者的AR表达也明显增加。此外,AO患者中JNK1的激活增加。雄激素可使健康受试者的ApoD表达增加,并伴有JNK1激活。抑制JNK1激活可能会降低AO患者中ApoD的表达以及雄激素诱导的ApopD表达。

结论

ApoD表达增加与AR信号通路密切相关。JNK1激活是AO患者中ApoD表达增加以及雄激素诱导的ApopD表达的主要原因。抑制JNK1激活可能会抑制AO患者内源性ApoD表达以及雄激素诱导的ApopD表达。

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