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K+ deficiency caused defects in renal tubular cell proliferation, oxidative stress response, tissue repair and tight junction integrity, but enhanced energy production, proteasome function and cellular K+ uptake.

Authors
  • Kapincharanon, Chompunoot1, 2, 3
  • Thongboonkerd, Visith1, 3
  • 1 a Medical Proteomics Unit, Office for Research and Development , Siriraj Hospital, Mahidol University , Bangkok , Thailand. , (Thailand)
  • 2 b Department of Immunology , Siriraj Hospital, Mahidol University , Bangkok , Thailand. , (Thailand)
  • 3 c Center for Research in Complex Systems Science , Mahidol University , Bangkok , Thailand. , (Thailand)
Type
Published Article
Journal
Cell Adhesion & Migration
Publisher
Landes Bioscience
Publication Date
May 04, 2018
Volume
12
Issue
3
Pages
247–258
Identifiers
DOI: 10.1080/19336918.2017.1356554
PMID: 28820294
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Hypokalemia is a common electrolyte disorder in hospitalized patients and those with chronic diseases and is associated with renal tubular injury. Our recent expression proteomics study revealed changes in levels of several proteins in renal tubular cells during K+ deficiency. However, functional significance and mechanisms underlying such changes remained unclear. The present study, thus, aimed to investigate functional changes of renal tubular cells induced by K+ deficiency. MDCK cells were maintained in normal-K+ (ANK; [K+] = 5.0 mM), Low-K+ (ALK; [K+] = 2.5 mM), or K+-depleted (AKD; [K+] = 0 mM) medium. Cell count and cell death assay showed that ALK and AKD groups had marked decrease in cell proliferation without significant change in cell death. Other functional investigations revealed that AKD cells had significantly increased levels of carbonylated proteins (by OxyBlot assay), impaired tissue repair (by scratch assay), defective tight junction (by Western blotting, immunofluorescence staining and measuring transepithelial electrical resistance), increased intracellular ATP level (by ATP measurement), decreased levels of ubiquitinated proteins (by Western blotting), and increased level of Na+/K+-ATPase (by Western blotting), which was consistent with the increased cellular K+ uptake after K+ repletion. Our findings have shown that AKD caused defects in cell proliferation, oxidative stress response, tissue repair and tight junction integrity, but on the other hand, enhanced energy production, proteasome function and cellular K+ uptake. These findings may shed light onto cellular response to K+ deficiency and better understanding of both pathogenic and compensatory mechanisms in hypokalemic nephropathy.

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