ID 112434
Author
Takase, Naoko Gifu Pharmaceutical University
Inden, Masatoshi Gifu Pharmaceutical University
Sekine, Shin-ichiro Gifu Pharmaceutical University
Ishii, Yumi Gifu Pharmaceutical University
Yonemitsu, Hiroko Gifu Pharmaceutical University
Iwashita, Wakana Gifu Pharmaceutical University
Kurita, Hisaka Gifu Pharmaceutical University
Hozumi, Isao Gifu Pharmaceutical University
Content Type
Journal Article
Description
PiT-1 (encoded by SLC20A1) and PiT-2 (encoded by SLC20A2) are type-III sodium-dependent phosphate cotransporters (NaPiTs). Recently, SLC20A2 mutations have been found in patients with idiopathic basal ganglia calcification (IBGC), and were predicted to bring about an inability to transport Pi from the extracellular environment. Here we investigated the effect of low Pi loading on the human neuroblastoma SH-SY5Y and the human glioblastoma A172 cell lines. The results show a different sensitivity to low Pi loading and differential regulation of type-III NaPiTs in these cells. We also examined whether 5-aminolevulinic acid (5-ALA) inhibited low Pi loading-induced neurotoxicity in SH-SY5Y cells. Concomitant application of 5-ALA with low Pi loading markedly attenuated low Pi-induced cell death and mitochondrial dysfunction via the induction of HO-1 by p38 MAPK. The findings provide us with novel viewpoints to understand the pathophysiology of IBGC, and give a new insight into the clinical prevention and treatment of IBGC.
Journal Title
Scientific Reports
ISSN
20452322
Publisher
Springer Nature
Volume
7
Start Page
5768
Published Date
2017-07-18
Remark
Supplementary Data : srep_7_5768_s1.pdf
Rights
© The Author(s) 2017
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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language
eng
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departments
Medical Sciences