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.
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.
Authors: Gail A Greendale; Jian Chu; Robert Ferrell; John F Randolph; Janet M Johnston; MaryFran R Sowers Journal: Am J Med Date: 2006-09 Impact factor: 4.965