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Ochratoxin A exerts neurotoxicity in human astrocytes through mitochondria-dependent apoptosis and intracellular calcium overload

Authors
Park, SunwooLim, WhasunYou, SeungkwonSong, Gwonhwa
Issue Date
1-10월-2019
Publisher
ELSEVIER IRELAND LTD
Keywords
Ochratoxin A; Astrocyte; Proliferation; Apoptosis; Toxicity
Citation
TOXICOLOGY LETTERS, v.313, pp.42 - 49
Indexed
SCIE
SCOPUS
Journal Title
TOXICOLOGY LETTERS
Volume
313
Start Page
42
End Page
49
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/62569
DOI
10.1016/j.toxlet.2019.05.021
ISSN
0378-4274
Abstract
Astrocytes are the major glial cell type in the central nervous system (CNS), and the distal part of the astrocyte forms the blood-brain barrier with nearby blood vessels. They maintain the overall metabolism, growth, homeostasis of neurons, and signaling in the CNS. Ochratoxin A is considered a carcinogen and immunotoxic, nephrotoxic, and neurotoxic mycotoxin. Specifically, it exhibits neurotoxicity with high affinity for the brain. Despite some previous studies about the effects of ochratoxin A in glial cells, the intracellular working mechanism in astrocytes is not fully understood. In this study, we studied the specific working mechanism of ochratoxin A in the human astrocyte cell line, NHA-SV40LT. Ochratoxin A reduced cell proliferation with sub G0/G1 cell cycle arrest by inhibiting CCND1, CCNE1, CDK4, and MYC expression. It induced apoptosis of NHA-SV40LT cells through mitochondrial membrane potential (MMP) loss and up-regulation of BAX and TP53. In addition, ochratoxin A increased cytosolic and mitochondrial calcium levels, resulting in an increase in MMP2 and PLAUR mRNA expression in NHA-SV40LT cells. Furthermore, ochratoxin A regulated the phosphorylation of AKT, ERK1/2, and JNK signal molecules of human astrocytes. Collectively, ochratoxin A exerts neurotoxicity through anti-proliferation and mitochondria-dependent apoptosis in human astrocytes.
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생명과학대학 (생명공학부)
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