Artemin transiently increases iNOS expression in primary cultured trigeminal ganglion neurons. (1st November 2017)

• Record Type: Journal Article
• Authors: Shang, Haiqiong; Wang, Yan; Chao, Xiuhua; Sun, Gaoying; Bai, Xiaohui; Xu, Lei; Han, Yuechen; Li, Jianfeng; Wang, Haibo; Fan, Zhaomin
• Is Part Of: Neuroscience letters. Volume 660(2017)
• Page Start: 34
• Page End: 38
• Publication Date: 2017-11-01
• Subjects: Artemin -- Trigeminal ganglion -- iNOS -- GFRα3 -- TUJ-1; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.09.016
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: The protein expression of iNOS is increased in primary cultured trigeminal ganglion neurons (TGNs) after artemin treatment. Fluorescence expression of iNOS is enhanced in TGNs after artemin treatment. Artemin-induced iNOS expression is co-localized with GFRα3 and TUJ-1, respectively. Abstract: Artemin, a member of the glial cell line-derived neurotrophic factor family, is an important cytokine and a critical participant in trigeminal pain disorders such as tongue pain and migraine. However, the mechanisms underlying artemin's activity are largely unknown. In the present study, we used primary cultured trigeminal ganglion neurons (TGNs) to determine the effect of artemin on the expression of the inducible form of nitric oxide synthase (iNOS), which is released in response to painful and inflammatory stimuli. Following artemin treatment, western blot analysis showed that the protein level of iNOS was transiently elevated after artemin treatment for 15 min ( p < 0.05). Immunofluorescence revealed that both the expressions of iNOS and GFRα3 were significantly up-regulated after artemin treatment for 15 min. In addition, iNOS expression induced by artemin was co-localized with GFRα3 and TUJ-1 in primary cultured TGNs, respectively. Our results indicate a previously unknown role of artemin in regulating iNOS expression in primary cultured TGNs, and regulation of iNOS might be involved in the mechanism through which artemin participates in the trigeminal pain pathway.