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Hypertonic sodium choloride and mannitol induces COX-2 via different signaling pathways in mouse cortical collecting duct M-1 cells

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dc.contributor.authorLim, WonChung-
dc.contributor.authorJung, JinSup-
dc.contributor.authorSurh, Youngjoon-
dc.contributor.authorInoue, Hiroyasu-
dc.contributor.authorLee, YoungJoo-
dc.date.accessioned2021-01-31T10:18:51Z-
dc.date.available2021-01-31T10:18:51Z-
dc.date.issued2007-05-
dc.identifier.citationLife Sciences, Vol.80 No.22, pp.2085-2092-
dc.identifier.issn0024-3205-
dc.identifier.other6282-
dc.identifier.urihttps://hdl.handle.net/10371/172815-
dc.description.abstractThe kidney cortical collecting duct is an important site for the maintenance of sodium balance. Previous studies have shown that, in renal medullary cells, hypertonic stress induces expression of cyclooxygenase-2 (COX-2) via NF-kappa B activation, but little is known about COX-2 expression in response to hypertonicity in the cortical collecting duct. Therefore, we examined the mechanism of hypertonic induction of COX-2 in M-1 cells derived from mouse cortical collecting duct. Induction of COX-2 protein was detected within 6 h of treatment with hypertonic sodium chloride. The treatment also increased COX-2 mRNA accumulation in a cycloheximide-independent manner, suggesting that ongoing protein synthesis is not required for COX-2 induction. Using reporter plasmids containing 0.2-, 0.3-, and 1.5-kb fragments of the COX-2 promoter, we found that hypertonic induction of COX-2 was due to an increase in promoter activity. The COX-2-inductive effect of hypertonicity was inhibited by SB203580, indicating that the effect is mediated by p38 MAPK. Since p38 MAPK can activate NF-kappa B, we made point mutations in the NF-kappa B binding site within the COX-2 promoter. The mutations did not block the induction of COX-2 promoter activity by hypertonic sodium chloride, and hypertonic sodium chloride failed to activate NF-kappa B binding site-driven reporter gene constructs. In contrast, hypertonic mannitol activated NF-kappa B, indicating that hypertonic mannitol and hypertonic sodium chloride activate COX-2 by different mechanisms. Thus, induction of COX-2 expression in M-1 cells by hypertonic sodium chloride does not involve activation of NF-kappa B. Furthermore, the signal transduction pathways that respond to hypertonic stress vary for different osmolytes in cortical collecting duct cells. (c) 2007 Elsevier Inc. All rights reserved.-
dc.subjectkidney cortical collecting duct-
dc.subjecthypertonicity-
dc.subjectcyclooxygenase-2-
dc.subjectNF-kappa B-
dc.titleHypertonic sodium choloride and mannitol induces COX-2 via different signaling pathways in mouse cortical collecting duct M-1 cells-
dc.typeArticle-
dc.contributor.AlternativeAuthor서영준-
dc.identifier.doi10.1016/j.lfs.2007.03.014-
dc.citation.journaltitleLife Sciences-
dc.identifier.scopusid2-s2.0-34247557479-
dc.citation.endpage2092-
dc.citation.number22-
dc.citation.startpage2085-
dc.citation.volume80-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0024320507002718?via%3Dihub-
dc.identifier.rimsid6282-
dc.identifier.sci000246924800011-
Appears in Collections:
Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
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