Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells.
Acute kidney injury (AKI) is characterized by a sudden loss of renal function. Early recognition of AKI, especially in critically ill patients, is essential for adequate therapy. Currently, neutrophil gelatinase-associated lipocalin (NGAL) is considered to be an effective biomarker of AKI; however,...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2016-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC5112913?pdf=render |
| _version_ | 1828879501435600896 |
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| author | Tadayoshi Konno Rei Nakano Ryo Mamiya Hisashi Tsuchiya Taku Kitanaka Shinichi Namba Nanako Kitanaka Ken Okabayashi Takanori Narita Hiroshi Sugiya |
| author_facet | Tadayoshi Konno Rei Nakano Ryo Mamiya Hisashi Tsuchiya Taku Kitanaka Shinichi Namba Nanako Kitanaka Ken Okabayashi Takanori Narita Hiroshi Sugiya |
| author_sort | Tadayoshi Konno |
| collection | DOAJ |
| description | Acute kidney injury (AKI) is characterized by a sudden loss of renal function. Early recognition of AKI, especially in critically ill patients, is essential for adequate therapy. Currently, neutrophil gelatinase-associated lipocalin (NGAL) is considered to be an effective biomarker of AKI; however, the regulation of its expression and function in renal tubular cells remains unclear. In this study, we investigated the regulation of the expression and function of NGAL in IL-1β-treated Madin-Darby canine kidney (MDCK) cells as a model of renal tubular cells. IL-1β induced a disturbance in the localization of E-cadherin and zonaoccludin-1 (ZO-1). The transepithelial electrical resistance (TER) also decreased 5 days after IL-1β treatment. IL-1β induced NGAL mRNA expression and protein secretion in a time- and dose-dependent manner, which occurred faster than the decrease in TER. In the presence of ERK1/2 and p38 inhibitors, IL-1β-induced NGAL mRNA expression and protein secretion were significantly attenuated. In the presence of recombinant NGAL, IL-1β-induced disturbance in the localization of E-cadherin and ZO-1 was attenuated, and the decrease in TER was partially maintained. These results suggest that NGAL can be used as a biomarker for AKI and that it functions as a protector from AKI. |
| first_indexed | 2024-12-13T09:29:33Z |
| format | Article |
| id | doaj.art-a8a089eb0f444e57a9d2882825598299 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-13T09:29:33Z |
| publishDate | 2016-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-a8a089eb0f444e57a9d28828255982992022-12-21T23:52:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-011111e016670710.1371/journal.pone.0166707Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells.Tadayoshi KonnoRei NakanoRyo MamiyaHisashi TsuchiyaTaku KitanakaShinichi NambaNanako KitanakaKen OkabayashiTakanori NaritaHiroshi SugiyaAcute kidney injury (AKI) is characterized by a sudden loss of renal function. Early recognition of AKI, especially in critically ill patients, is essential for adequate therapy. Currently, neutrophil gelatinase-associated lipocalin (NGAL) is considered to be an effective biomarker of AKI; however, the regulation of its expression and function in renal tubular cells remains unclear. In this study, we investigated the regulation of the expression and function of NGAL in IL-1β-treated Madin-Darby canine kidney (MDCK) cells as a model of renal tubular cells. IL-1β induced a disturbance in the localization of E-cadherin and zonaoccludin-1 (ZO-1). The transepithelial electrical resistance (TER) also decreased 5 days after IL-1β treatment. IL-1β induced NGAL mRNA expression and protein secretion in a time- and dose-dependent manner, which occurred faster than the decrease in TER. In the presence of ERK1/2 and p38 inhibitors, IL-1β-induced NGAL mRNA expression and protein secretion were significantly attenuated. In the presence of recombinant NGAL, IL-1β-induced disturbance in the localization of E-cadherin and ZO-1 was attenuated, and the decrease in TER was partially maintained. These results suggest that NGAL can be used as a biomarker for AKI and that it functions as a protector from AKI.http://europepmc.org/articles/PMC5112913?pdf=render |
| spellingShingle | Tadayoshi Konno Rei Nakano Ryo Mamiya Hisashi Tsuchiya Taku Kitanaka Shinichi Namba Nanako Kitanaka Ken Okabayashi Takanori Narita Hiroshi Sugiya Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells. PLoS ONE |
| title | Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells. |
| title_full | Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells. |
| title_fullStr | Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells. |
| title_full_unstemmed | Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells. |
| title_short | Expression and Function of Interleukin-1β-Induced Neutrophil Gelatinase-Associated Lipocalin in Renal Tubular Cells. |
| title_sort | expression and function of interleukin 1β induced neutrophil gelatinase associated lipocalin in renal tubular cells |
| url | http://europepmc.org/articles/PMC5112913?pdf=render |
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