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Toshiaki Hitomi

As seen in: PLOS ONE, MDPI
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Articles

Interaction of coexposure to inorganic arsenic and manganese: Tight junction injury of the blood-brain barrier and the relationship between oxidative stress and inflammatory cytokines in glial cells | PLOS One

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By Toshiaki Hitomi, Hiroko Okuda, Ayako Takata, Hiroshi Yamauchi
| PLOS ONE
Loading metrics Open Access Peer-reviewed Research Article Citation: Hitomi T, Okuda H, Takata A, Yamauchi H (2025) Interaction of coexposure to inorganic arsenic and manganese: Tight junction injury of the blood–brain barrier and the relationship between oxidative stress and inflammatory cytokines in glial cells. PLoS One 20(8): e0330287. https://doi.org/10.1371/journal.pone.0330287 Editor: Mária A.
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Evaluation of arsenic metabolism and tight junction injury after exposure to arsenite and monomethylarsonous acid using a rat in vitro blood-Brain barrier model | PLOS ONE

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By Hiroshi Yamauchi, Toshiaki Hitomi, Ayako Takata
| PLOS ONE
Loading metrics Open Access Peer-reviewed Research Article Citation: Yamauchi H, Hitomi T, Takata A (2023) Evaluation of arsenic metabolism and tight junction injury after exposure to arsenite and monomethylarsonous acid using a rat in vitro blood–Brain barrier model. PLoS ONE 18(11): e0295154. https://doi.org/10.1371/journal.pone.0295154 Editor: Mária A.
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Biochemical and Functional Characterization of RNF213 (Mysterin) R4810K, a Susceptibility Mutation of Moyamoya Disease, in Angiogenesis In Vitro and In Vivo

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By Hatasu Kobayashi, Yoshiko Matsuda, Toshiaki Hitomi, Hiroko Okuda, Hirotomo Shioi, Tetsuya Matsuda, Hirohiko Imai, Masakatsu Sone, Daisuke Taura, Kouji H. Harada, Toshiyuki Habu, Yasushi Takagi, Susumu Miyamoto
| jaha.ahajournals.org
Methods and Results To clarify the role of RNF213 in known angiogenic pathways, RNF213 expression was analyzed in endothelial cells (ECs) treated with several angiogenic and antiangiogenic factors, including interferons (IFNs). RNF213 was upregulated by IFN‐β through signal transducer and activator of transcription x in the promoter and mediated antiangiogenic activity of IFN‐β. RNF213 wild‐type (WT) overexpression could not lower angiogenesis without IFN‐β, but RNF213 R4810K overexpression could.
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