Long-term dexamethasone treatment diminishes store-operated Ca^(2+) entry in salivary acinar cells  

作　　者：Yuichiro Kusuda Yusuke Kondo Yuta Miyagi Takashi Munemasa Yusuke Hori Fumiko Aonuma Shintaro Tsuka Taro Mukaibo Chihiro Masaki Ryuji Hosokawa 

机构地区：[1]Division of Oral Reconstruction and Rehabilitation, Kyushu Dental University

出　　处：《International Journal of Oral Science》2019年第1期25-32,共8页国际口腔科学杂志（英文版）

基　　金：supported by a grant from the Japan Society for the Promotion of Science KAKENHI (No. 17K17184)

摘　　要：Corticosteroids are used in the treatment of many diseases; however, they also induce various side effects. Dexamethasone is one of the most potent corticosteroids, and it has been reported to induce the side effect of impaired salivary gland function. This study aimed to evaluate the effects of dexamethasone on mouse submandibular gland function to gain insight into the mechanism of dexamethasone-induced salivary hypofunction. The muscarinic agonist carbachol(CCh) induced salivary secretion and was not affected by short-term dexamethasone treatment but was decreased following long-term dexamethasone administration. The expression levels of the membrane proteins Na^+-K^+-2 Cl-cotransporter, transmembrane member 16 A, and aquaporin 5 were comparable between the control and long-term dexamethasone treatment groups. The CCh-induced increase in calcium concentration was significantly lower in the presence of extracellular Ca^(2+) in the long-term dexamethasone treatment group compared to that in the control group. Furthermore, CCh-induced salivation in the absence of extracellular Ca^(2+) and Ca^(2+) ionophore A23187-induced salivation was comparable between the control and long-term dexamethasone treatment groups.Moreover, salivation induced by the Ca^(2+) -ATPase inhibitor thapsigargin was diminished in the long-term dexamethasone treatment group. In summary, these results demonstrate that short-term dexamethasone treatment did not impair salivary gland function, whereas long-term dexamethasone treatment diminished store-operated Ca^(2+) entry, resulting in hyposalivation in mouse submandibular glands.Corticosteroids are used in the treatment of many diseases; however, they also induce various side effects. Dexamethasone is one of the most potent corticosteroids, and it has been reported to induce the side effect of impaired salivary gland function. This study aimed to evaluate the effects of dexamethasone on mouse submandibular gland function to gain insight into the mechanism of dexamethasone-induced salivary hypofunction. The muscarinic agonist carbachol(CCh) induced salivary secretion and was not affected by short-term dexamethasone treatment but was decreased following long-term dexamethasone administration. The expression levels of the membrane proteins Na^+-K^+-2 Cl-cotransporter, transmembrane member 16 A, and aquaporin 5 were comparable between the control and long-term dexamethasone treatment groups. The CCh-induced increase in calcium concentration was significantly lower in the presence of extracellular Ca^(2+) in the long-term dexamethasone treatment group compared to that in the control group. Furthermore, CCh-induced salivation in the absence of extracellular Ca^(2+) and Ca^(2+) ionophore A23187-induced salivation was comparable between the control and long-term dexamethasone treatment groups.Moreover, salivation induced by the Ca^(2+) -ATPase inhibitor thapsigargin was diminished in the long-term dexamethasone treatment group. In summary, these results demonstrate that short-term dexamethasone treatment did not impair salivary gland function, whereas long-term dexamethasone treatment diminished store-operated Ca^(2+) entry, resulting in hyposalivation in mouse submandibular glands.

关 键 词：CORTICOSTEROIDS carbachol(CCh)induced 

分 类 号：R[医药卫生]