Expression of prostanoid receptors (EP1, 2, 3, and 4) in normal and methimazole-treated mouse olfactory epithelium.

CONCLUSION: Prostanoid receptors (EP1, EP2, EP3, and EP4) are expressed in the olfactory epithelium (OE), and the EP4 prostanoid receptor may play an important role in the OE. OBJECTIVE: The purpose of the present study was to investigate the expression and localization of the four types of prostanoid receptors (EP1, EP2, EP3, and EP4) in the OE of normal and methimazole-treated mice to gain more complete knowledge about the functional significance of the prostanoid receptors in OE. METHODS: CBA/J mice were used in this study. The localization of the prostanoid receptors (EP1, EP2, EP3, and EP4) in the OE was investigated by immunohistochemistry. The changes in expression of prostanoid receptors were studied in methimazole-treated mice. Furthermore, the effect of EP agonists on the methimazole-induced degeneration of OE was assessed by morphological analysis and by assessment of apoptosis. RESULTS: All four types of EP receptors were recognized in mouse OE. Expression of EP4 in the OE was significantly reduced after methimazole treatment. In the methimazole-treated mice, an EP4 agonist reduced OE damage and apoptosis.

Expression of transient receptor potential channel vanilloid (TRPV) 1–4, melastin (TRPM) 5 and 8, and ankyrin (TRPA1) in the normal and methimazole-treated mouse olfactory epithelium.

CONCLUSION: It is suggested that TRPV1, 2, 3, and 4, TRPM5 and 8, and TRPA1 may play several roles in the olfactory epithelium (OE), contributing to olfactory chemosensation, olfactory adaptation, olfactory­trigeminal interaction, and OE fluid homeostasis. In patients with olfactory disturbance, TRPV1 and TRPM8 may be closely related to a high rate of recognition of curry and menthol odors, while TRPV2 may also play a crucial role in the regeneration of olfactory receptor neurons. OBJECTIVE: Expression of TRPV1­4, TRPM5 and 8, and TRPA1 in the normal and methimazole-treated mouse OE was analyzed. METHODS: The localization of TRPV1­4, TRPM5 and 8, and TRPA1 in the OE of normal and methimazole-treated CBA/J mice was investigated by immunohistochemistry. RESULTS: Normal OE showed a positive immunofluorescent reaction to TRPV1­4, TRPM5 and 8, and TRPA1. In lamina propria, the nerve fibers displayed TRPV 1, 2, and 3, TRPM8 and TRPA1. In the pathological condition, the expression of TRPV3, TRPV4, TRPM5, and TRPA1 was markedly reduced and took a long time to recover. In contrast, expression of TRPM8 was scarcely affected, even in the pathological condition, while TRPV1 and TRPV2 showed early recovery following methimazole treatment.

Analysis of syndecan-1 and TGF-beta expression in the nasal mucosa and nasal polyps.

OBJECTIVE: Increased understanding of cytokines and their associated proteoglycans will contribute to the investigation of the formation of nasal polyps. Recently, some studies have suggested that syndecan-1 ectodomains are shed in response to low respiratory infection, but no studies regarding nasal and paranasal diseases have been reported. Transforming growth factor-beta (TGF-beta) is involved in the regulation of nasal polyps, especially in processes crucial to the initiation, maintenance, and resolution of inflammatory responses. In the nasal mucosa and nasal polyps, we analyzed the expression of syndecan-1, which readily promotes infection, and TGF-beta, which plays a role in syndecan-1 activity. METHODS: Fifteen patients who underwent turbinectomy for the treatment of nasal obstruction and seventeen patients with nasal polyps who underwent nasal endoscopic sinus surgery were included in this study. The localization of syndecan-1 and TGF-beta in the nasal mucosa and nasal polyps was investigated by immunohistochemistry, and mRNA transcript levels of syndecan-1 and TGF-beta were examined using quantitative real-time PCR. RESULTS: Immunohistochemical staining revealed that the expression of syndecan-1 in the nasal mucosa and nasal polyps was co-localized with TGF-beta. The mean mRNA expression values for syndecan-1 and TGF-beta were higher in nasal polyps compared to the nasal mucosa. CONCLUSIONS: This is the first report showing expression of syndecan-1 in the nasal mucosa and nasal polyps. In nasal polyps, syndecan-1 expression may be increased by an unknown mechanism, permitting infection and inducing larger nasal polyps. We hypothesize that the accumulation of TGF-beta, which is involved in the pathophysiological development of nasal polyps, may result in a change in the binding properties of syndecan-1 at inflammatory sites.