Endocrine Abstracts

Introduction: Dexamethasone inhibits mucin secretion considering the primary option for treating acute asthma exacerbation. However, the mechanism underlying dexamethasone-induced decreased in mucosecretion is unclear. Recent studies have reported that dexamethasone exerts an inhibitory effect on mucosecretion in the lung by modulating the expression of calcium-processing genes. However, the expression of the calcium-processing genes in trachea are not examined yet. Thus, the present study is the first to report glucocorticoid-induced regulation of calcium processing genes such as transient receptor potential vanilloid-4 (Trpv4), transient receptor potential vanilloid-6 (Trpv6), calbindin-D_9k (CaBP-9k), and plasma membrane Ca²⁺-ATPase (Pmca1) in the mouse trachea.

Materials and methods: In this study, mice were subcutaneously injected with dexamethasone for 5 days, or injected with estradiol or progesterone for 3 days. The tracheal tissues were collected by dividing the trachea into cervical and thoracic sections based on its anatomical structure. Real-time PCR was performed to investigate mRNA expression of calcium-processing genes. Immunohistochemistry and immunofluorescence were performed to localize the calcium-processing proteins. Tracheal mucosubstances were detected by performing Alcian blue-periodic acid-Schiff staining.

Results: The localization of TRPV4, TRPV6, CaBP-9k, and PMCA1 proteins was detected in the tracheal epithelium, submucosal glands, cartilages and muscles. Dexamethasone treatment downregulated the mRNA expression of the four calcium-processing genes and mucin 1, mucin 4, mucin 5ac, and mucin 5b genes. Dexamethasone decrease in the secretion of mucosubstances in the trachea.

Conclusions: The findings of the present study suggest that glucocorticoids regulate the tracheal expression of calcium-processing genes and tracheal mucosecretion.