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Affiliation |
Faculty of Medicine School of Medicine Department of Anatomy, Ultrastructural Cell Biology |
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Assistant Professor |
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Related SDGs |
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KITAGAWA Kyoko
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Papers 【 display / non-display 】
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Kitagawa K., Shibata E., Yamamoto M., Harada H., Yoshino K., Iwashita T., Oshima M., Tsuji M.
Genes to Cells 28 ( 1 ) 42 - 52 2023.1
Authorship：Lead author, Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Genes to Cells
Bisphenol F diglycidyl ether (BFDGE) is widely used in the synthesis process of plastic products. While exposure to bisphenol A diglycidyl ether (BADGE), which has a similar structure to BFDGE and which is used for the same purpose, has been reported to cause health risks, there is still little information on BFDGE. Because it is estimated that the industrial workers are exposed to large amounts of BFDGE, the health risks associated with BFDGE exposure need to be clarified. We investigated the toxicity of cutaneous exposure to BFDGE using an in vitro evaluation system and a mouse exposure model. The tumorigenic potential of BFDGE was confirmed by the Bhas 42 cell transformation assay, which showed that BFDGE has both promoter and initiator activity, in vitro. A single dermal application of BFDGE was associated with minor contact hypersensitivity symptoms. In contrast, repeated dermal exposure to BFDGE for 2 weeks induced persistent acute inflammation with features similar to inflammation in human psoriasis. This is the first report evaluating the toxicity of BFDGE in animals, and we showed that BFDGE carries a health risk of inducing skin dermatitis similar to that in human psoriasis in an exposure period-dependent manner.
DOI： 10.1111/gtc.12995
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Kitagawa K., Uchida C., Horiguchi R., Ohhata T., Sakai S., Niida H., Yasumoto S., Handa Y., Suzuki M., Hashimoto M., Tazawa T., Yokochi Y., Tsuji M., Kitagawa M.
Scientific Reports 10 ( 1 ) 14381 2020.12
Authorship：Lead author, Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Scientific Reports
The expression level of transcription factor c-Myb oscillates during hematopoiesis. Fbw7 promotes ubiquitin-mediated degradation of c-Myb, which is dependent on phosphorylation of Thr572. To investigate the physiological relevance of Fbw7-mediated c-Myb degradation, we generated mutant mice carrying c-Myb-T572A (TA). Homozygous mutant (TA/TA) mice exhibited a reduction in the number of peripheral red blood cells and diminished erythroblasts in bone marrow, presumably as a result of failure during erythroblast differentiation. We found that c-Myb high-expressing cells converged in the Lin−CD71+ fraction, and the expression of c-Myb was higher in TA/TA mice than in wild-type mice. Moreover, TA/TA mice had an increased proportion of the CD71+ subset in Lin− cells. The c-Myb level in the Lin−CD71+ subset showed three peaks, and the individual c-Myb level was positively correlated with that of c-Kit, a marker of undifferentiated cells. Ultimately, the proportion of c-Mybhi subgroup was significantly increased in TA/TA mice compared with wild-type mice. These results indicate that a delay in reduction of c-Myb protein during an early stage of erythroid differentiation creates its obstacle in TA/TA mice. In this study, we showed the T572-dependent downregulation of c-Myb protein is required for proper differentiation in early-stage erythroblasts, suggesting the in vivo significance of Fbw7-mediated c-Myb degradation.
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Largescale semithin sectioning method supported by a stainless steel ring enables multiscale analysis in transmission electron microscopy. Reviewed
Takahashi N, Kitagawa K, Nagashima Y, Imazato H, Sawaguchi A
Scientific reports 2026.7
Language：English Publishing type：Research paper (scientific journal)
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Caregiver-initiated food avoidance and risk of iron deficiency anemia in early childhood: Evidence from the Japan environment and children's study. Reviewed
Tanaka R, Tsuji M, Ishitsuka K, Sakuragi T, Kitagawa K, Kuwamura M, Suga R, Araki S, Maruyama T, Eguchi H, Shibata E, Morokuma S, Shimono M, Yoshino K, Hamada N, Ochiai M, Ohga S, Kusuhara K, Japan Environment and Children's Study (JECS) Group
Nutrition and health 2601060261461106 2026.7
Language：English Publishing type：Research paper (scientific journal)
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Kuwamura M., Tanaka K., Onoda A., Taki K., Koriyama C., Kitagawa K., Kawamoto T., Tsuji M.
BMC Pediatrics 24 ( 1 ) 26 2024.12
Language：English Publishing type：Research paper (scientific journal) Publisher：BMC Pediatrics
Background: Bisphenol A diglycidyl ether (BADGE) and Bisphenol F diglycidyl ether (BFDGE) are used in medical devices, such as intravenous sets, syringes, and catheters. Several studies have reported that these compounds are endocrine disruptors, cytotoxic, and genotoxic, raising concerns about their adverse effects on infants, in a stage of remarkable growth and development. The present study aimed to measure the serum concentrations of BADGE, derivatives of BADGE, and BFDGE in infants and examine the factors that influence them. Methods: Ten infants admitted to the neonatal intensive care unit (NICU) were enrolled in the present study. Blood samples from each infant and questionnaires from their mothers were collected twice, at 1–2 months and 7 months of age. BADGE, BADGE·H2O, BADGE·2H2O, and BFDGE were quantified using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Results: Serum BADGE·2H2O was identified in all infants, at both 1–2 months (2.30–157.58 ng/ml) and 7 months of age (0.86–122.85 ng/ml). One of the two infants who received invasive ventilation showed a substantially increased BADGE·2H2O concentration. There was no significant difference in BADGE·2H2O concentrations at 7 months of age between the group that ate commercial baby food at least ≥ 1 time per week and the group that did not. Conclusions: BADGE·2H2O was detected in the serum of all infants with a history of NICU hospitalization. Future studies are needed to determine the source of BADGE exposure and investigate its effects on infant development.
Grant-in-Aid for Scientific Research 【 display / non-display 】
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ゲノム編集オルガノイド由来プレクニカルモデルによるスキルス胃がん発生進展の解明
Grant number：23K06662 2023.04 - 2026.03
独立行政法人日本学術振興会 科学研究費基金 基盤研究(C)
Authorship：Principal investigator