Developmental Exposure of Mice to T-2 Toxin Increases Astrocytes and Hippocampal Neural Stem Cells Expressing Metallothionein View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-04

AUTHORS

Kota Nakajima, Takeshi Tanaka, Yasunori Masubuchi, Yuko Ito, Satomi Kikuchi, Gye-Hyeong Woo, Toshinori Yoshida, Makoto Shibutani

ABSTRACT

We previously reported that developmental exposure to T-2 toxin caused transient disruption of the hippocampal neurogenesis targeting neural stem cells (NSCs) and early-stage progenitor cells involving oxidative stress on weaning in mouse offspring. The present study examined metallothionein (MT) expression changes and their cellular identity in brain regions of these animals. T-2 toxin at 0, 1, 3, and 9 mg/kg was given in the diet of maternal mice from gestational day 6 to postnatal day (PND) 21 on weaning. Offspring were maintained through PND 77 without T-2 toxin exposure. Male offspring were analyzed. Immunohistochemically, MT-I/II+ cells increased in the subgranular zone (SGZ) of the dentate gyrus and cerebral cortex at ≥ 3 mg/kg and in the hilus of the dentate gyrus, corpus callosum, and cerebellum at 9 mg/kg on PND 21, suggestive of operation of cytoprotective function against oxidative stress throughout the brain. Double immunohistochemistry analysis revealed MT-I/II+ SGZ cells to be NSCs and MT-I/II+ cells in other brain regions to be astrocytes as toxicity targets of T-2 toxin. Phosphorylated STAT3+ cell numbers increased only in the cerebellum in parallel with the increase of GFAP+ astrocytes at 9 mg/kg, suggesting a STAT3-mediated transcriptional GFAP upregulation in cerebellar astrocytes. In the dentate gyrus, Il1a, Il1r1, and Mt2 increased transcripts at 9 mg/kg, suggesting activation of the IL-1 signaling cascade, possibly causing MT-II upregulation. The increase of MT-I/II+ cells in all brain regions disappeared or was suppressed below the control level on PND 77, suggesting a recovery from the T-2 toxin-induced oxidative stress. More... »

PAGES

668-683

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12640-018-9981-4

DOI

http://dx.doi.org/10.1007/s12640-018-9981-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1110263902

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30488313


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254 schema:name Cooperative Division of Veterinary Sciences, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, 183-8509, Fuchu-shi, Tokyo, Japan
255 Institute of Global Innovation Research, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, 183-8509, Fuchu-shi, Tokyo, Japan
256 Laboratory of Veterinary Pathology, Division of Animal Life Science, Institute of Agriculture, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, 183-8509, Fuchu-shi, Tokyo, Japan
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258 https://www.grid.ac/institutes/grid.256342.4 schema:alternateName Gifu University
259 schema:name Laboratory of Veterinary Pathology, Division of Animal Life Science, Institute of Agriculture, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, 183-8509, Fuchu-shi, Tokyo, Japan
260 Pathogenetic Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, 501-1193, Gifu-shi, Gifu, Japan
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262 https://www.grid.ac/institutes/grid.443977.a schema:alternateName Semyung University
263 schema:name Laboratory of Histopathology, Department of Clinical Laboratory Science, Semyung University, 65 Semyung-ro, 27136, Jecheon-si, Chungbuk, Republic of Korea
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