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Ca(2+) is a Regulator of the WNK/OSR1/NKCC Pathway in a Human Salivary Gland Cell Line

Authors
 Soonhong Park  ;  Sang Kyun Ku  ;  Hye Won Ji  ;  Jong Hoon Choi  ;  Dong Min Shin 
Citation
 KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.19(3) : 249-255, 2015 
Journal Title
 KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY 
ISSN
 1226-4512 
Issue Date
2015
Keywords
Ca2+ signaling ; NKCC ; OSR1 ; Salivary gland ; WNK
Abstract
Wnk kinase maintains cell volume, regulating various transporters such as sodium-chloride cotransporter, potassium-chloride cotransporter, and sodium-potassium-chloride cotransporter 1 (NKCC1) through the phosphorylation of oxidative stress responsive kinase 1 (OSR1) and STE20/SPS1-related proline/alanine-rich kinase (SPAK). However, the activating mechanism of Wnk kinase in specific tissues and specific conditions is broadly unclear. In the present study, we used a human salivary gland (HSG) cell line as a model and showed that Ca(2+) may have a role in regulating Wnk kinase in the HSG cell line. Through this study, we found that the HSG cell line expressed molecules participating in the WNK-OSR1-NKCC pathway, such as Wnk1, Wnk4, OSR1, SPAK, and NKCC1. The HSG cell line showed an intracellular Ca(2+) concentration ([Ca(2+)]i) increase in response to hypotonic stimulation, and the response was synchronized with the phosphorylation of OSR1. Interestingly, when we inhibited the hypotonically induced [Ca(2+)]i increase with nonspecific Ca(2+) channel blockers such as 2-aminoethoxydiphenyl borate, gadolinium, and lanthanum, the phosphorylated OSR1 level was also diminished. Moreover, a cyclopiazonic acid-induced passive [Ca(2+)]i elevation was evoked by the phosphorylation of OSR1, and the amount of phosphorylated OSR1 decreased when the cells were treated with BAPTA, a Ca(2+) chelator. Finally, through that process, NKCC1 activity also decreased to maintain the cell volume in the HSG cell line. These results indicate that Ca(2+) may regulate the WNK-OSR1 pathway and NKCC1 activity in the HSG cell line. This is the first demonstration that indicates upstream Ca(2+) regulation of the WNK-OSR1 pathway in intact cells.
Files in This Item:
T201501331.pdf Download
DOI
10.4196/kjpp.2015.19.3.249
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Orofacial Pain and Oral Medicine (구강내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Park, Soon Hong(박순홍)
Shin, Dong Min(신동민) ORCID logo https://orcid.org/0000-0001-6042-0435
Ji, Hye Won(지혜원)
Choi, Jong Hoon(최종훈) ORCID logo https://orcid.org/0000-0003-3211-3619
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/140035
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