Long-term dexamethasone treatment diminishes store-operated Ca2+ entry in salivary acinar cells

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

International Journal of Oral Science ›› 2019, Vol. 11 ›› Issue (1) : 1

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International Journal of Oral Science ›› 2019, Vol. 11 ›› Issue (1) : 1 DOI: 10.1038/s41368-018-0031-0
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Long-term dexamethasone treatment diminishes store-operated Ca2+ entry in salivary acinar cells

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Abstract

Long-term corticosteroid use causes dry mouth by inhibiting calcium movement into salivary gland cells. Corticosteroid use is associated with multiple systemic side effects including salivary inhibition, prompting Yusuke Kondo and a research team from Japan’s Kyushu Dental University to elucidate the reasons why. Submandibular glands taken from mice after six weeks’ treatment with the corticosteroid dexamethasone produced significantly less saliva in ten minutes than a group given just one week’s treatment, or no treatment at all. Further investigation revealed that long-term dexamethasone treatment inhibited the ability of salivary gland cells, known as acinar cells, to transport calcium ions from the exterior to the interior of the cells—an essential mechanism enabling salivation. The study improves our understanding of corticosteroid-induced dry mouth and reveals potential pharmacological targets to enable treatment.

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Yuichiro Kusuda, Yusuke Kondo, Yuta Miyagi, Takashi Munemasa, Yusuke Hori, Fumiko Aonuma, Shintaro Tsuka, Taro Mukaibo, Chihiro Masaki, Ryuji Hosokawa. Long-term dexamethasone treatment diminishes store-operated Ca2+ entry in salivary acinar cells. International Journal of Oral Science, 2019, 11(1): 1 DOI:10.1038/s41368-018-0031-0

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Funding

Japan Society for the Promotion of Science (JSPS)(17K17184)

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