title: Increased JNK1 activity contributes to the upregulation of ApoD in the apocrine secretory gland cells from axillary osmidrosis.
abstract: Axillary osmidrosis is a benign disorder that causes functional and emotional problems in Asian patients. Recently, ApoD has been identified as an axillary odorant binding protein. The present study was designed to compare the expression of ApoD in normal and osmidrosis subjects. Compared with the normal subjects, osmidrosis subjects had a higher expression of AR and ApoD in the apocrine samples, both at mRNA and protein level. Further study showed that, consistent with the increased ApoD and AR, phosphorylated JNK1 was higher in apocrine samples from axillary osmidrosis subjects, while with no obvious differences of the total expression of JNK1. In the cultured apocrine epithelial cells from normal subjects, 5α-dihydrotestosterone (5α-DHT) increased the expression of ApoD in a dose dependent manner, which can be inhibited by the JNK1 inhibitor. In contrast, in the cultured apocrine epithelial cells from axillary osmidrosis subjects, inhibition of JNK1 significantly reduced the expression of ApoD. Taken together, our study here revealed that increased JNK1 activation in the apocrine cells from axillary osmidrosis contributes to the increased ApoD expression, which in turn involved in the process of axillary osmidrosis.
authors.affiliation: Department of Plastic Surgery, Tang du Hospital, The Fourth Military Medical University, Tangdu Hospital, Xinshi Road No 1, Baqiao District, Xi'an, 710038 Shaanxi, China. yxmrtd@fmmu.edu.cn
authors.forename: Hui
authors.initials: H
authors.lastname: Chen
authors.forename: Yingli
authors.initials: Y
authors.lastname: Li
authors.forename: Jie
authors.initials: J
authors.lastname: Du
authors.forename: Yan
authors.initials: Y
authors.lastname: Cao
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Li
mesh_terms: D000873:Anthracenes / Q000494:pharmacology; D001050:Apocrine Glands / Q000378:metabolism / Q000473:pathology*; D053399:Apolipoproteins D / Q000235:genetics / Q000378:metabolism*; D001365:Axilla / Q000473:pathology* / Q000503:physiopathology; D016022:Case-Control Studies; D002478:Cells, Cultured; D013196:Dihydrotestosterone / Q000494:pharmacology; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008297:Male; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism*; D048055:Mitogen-Activated Protein Kinase 8 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D010766:Phosphorylation; D011944:Receptors, Androgen / Q000378:metabolism; D015398:Signal Transduction; D014158:Transcription, Genetic; D015854:Up-Regulation
chemical_list: C024328:APOD protein, human; D000873:Anthracenes; D053399:Apolipoproteins D; D006023:Glycoproteins; D026901:Membrane Transport Proteins; D011944:Receptors, Androgen; D013196:Dihydrotestosterone; C432165:pyrazolanthrone; D048055:Mitogen-Activated Protein Kinase 8