IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711
Int J Clin Exp Med 2013;6(7):497-503

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

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

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

Received May 27, 2013; Accepted June 23, 2013; Epub August 1, 2013; Published August 15, 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. (IJCEM1305018).

Keywords: Axillary osmidrosis, apolipoprotein D, c-Jun N-terminal kinase, expression regulation

Address correspondence to: Hui Chen, Deparment of Plastic Surgery and Burn, Tangdu, Hospital, The Fourth Military Medical
University, Xi’an 710038, China. Phone: 0086-029-84775936; E-mail: chenmed@yeah.net; yxmrtd@fmmu.edu.cn