Kagoshima University · Medical Care Center

Research keywordstaste bud structure・taste epithelium differentiation・Prox1 regulation・apoptosis inhibition・tamoxifen transcriptional switch

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• Hagimoto A., Koyanagi-Matsumura E., Oura N., Saito M., Tanaka T., Miura H. . Prox1 maintains taste bud structure via inhibition of apoptosis . Cell and Tissue Research403 (担当区分： 筆頭著者, 最終著者, 責任著者 記述言語： 英語 掲載種別： 学位論文（博士） 出版者・発行元： Cell and Tissue Research Taste buds are maintained by continuous cell renewal, receiving a steady influx of postmitotic cells from the surrounding epithelial region. Within taste buds, Type I, II, and III cells continuously differentiate from Type IV postmitotic precursor cells and are removed via apoptosis. These processes are likely governed by various transcription factors. Among the transcription factors expressed in taste buds, Prox1, a homeobox transcription factor, is the only factor expressed in all taste bud cells including precursor cells. However, its role in taste buds remains unclear. Here, we investigate the function of Prox1 in taste bud cell turnover using conditional knockout (cKO) mice. In Prox1 cKO mice, all Type I, II, and III cells were significantly reduced, resulting in approximately half the total cell number per taste bud compared to wild-type mice, while Type IV cell numbers remained comparable. Apoptosis of taste bud cells nearly doubled, leading to a shortened lifespan of taste bud cells. EdU pulse-labeling experiments revealed a biphasic decline in EdU(+) taste bud cells in Prox1 cKO mice, indicating that Prox1 knockout increases the fraction of cells that die shortly after differentiating into taste bud cells. The surviving cells still exhibited a shorter lifespan than that of wild-type mice. We also observed previously unreported structural alterations within taste buds caused by enhanced apoptosis using whole-mount analysis. These results demonstrate that Prox1 contributes to the maintenance of taste bud structure by regulating the lifespan of taste bud cells, highlighting its essential role in taste bud homeostasis. DOI： 10.1007/s00441-025-04040-7 Scopus PubMed
• Fujita M., Indo H., Abe H., Hagimoto A., Kirishima M., Suzuki H., Saijo H., Tanaka T. . Giant cell tumor of bone of the skull mimicking multicentric giant cell tumor of bone revealed after den担当区分： 筆頭著者, 最終著者, 責任著者 記述言語： 英語 掲載種別： 研究論文（学術雑誌） 出版者・発行元： Oral Radiology Giant cell tumor of the bone (GCTB) is a benign osseous neoplasm that primarily occurs in the epiphyses. Approximately 2% of GCTBs occur in the head and neck regions. Herein, we report a rare case of GCTB in the skull, which was discovered during a dental consultation. The patient was a 74-year-old man who had discomfort in the left temporomandibular joint for 3 months. During the initial visit, there were no remarkable clinical or radiological findings, and the patient was placed under observation. After 3 months, the patient was referred owing to a rapid, progressive swelling on the left side of the head. CT images revealed a slight area of contrast enhancement around the temporomandibular joint, where the patient initially experienced symptoms, but no definite mass was detected, whereas an expansive lesion with cortical thinning and erosion was identified in the left temporal region. Contrast-enhanced magnetic resonance imaging (MRI) revealed heterogeneous enhancement of the temporal lesion and a separate 10-mm lesion with similar enhancement on the inferior surface of the greater wing of the sphenoid bone. Aspiration biopsies of both lesions confirmed the diagnosis of GCTB. Initially, imaging raised the possibility of multicentric GCTB. Nevertheless, while the temporal lesion clearly originated from the bone, a characteristic feature of GCTB, the sphenoid lesion showed no evidence of an intraosseous origin on either CT or MRI. Therefore, this is a rare case of GCTB of the skull with a distinct progression pattern. DOI： 10.1007/s11282-025-00880-9 Scopus PubMed
• Oura N., Koyanagi-Matsumura E., Hagimoto A., Saito M., Saijo H., Miura H. . Tamoxifen triggers a transcriptional switch from proliferation to differentiation in the circumvallate taste epithel担当区分： 筆頭著者, 最終著者, 責任著者 記述言語： 英語 掲載種別： 学位論文（博士） 出版者・発行元： Scientific Reports The tamoxifen-inducible Cre-loxP system is an indispensable experimental tool in life sciences for inducing spatiotemporally controlled genetic recombination in the target tissues of living animals. The use of this technology is expected to increase in taste research. However, the direct effects of tamoxifen on taste buds remain largely unexplored. Here, we demonstrate that tamoxifen reduces cell supply to the taste buds in a dose-dependent manner. RNA sequencing of the circumvallate epithelium revealed that tamoxifen induced a transcriptional shift from proliferation to differentiation. The genes regulating the cell cycle were downregulated, whereas genes promoting the differentiation of epithelial cells and keratinocytes were upregulated. Within taste buds, Shh was downregulated in immature precursor cells, whereas cell type-specific genes were broadly upregulated in mature taste bud cells. Notably, transcription factors driving taste cell type differentiation, such as Pou2f3, Ascl1, and Nkx2-2, were induced, suggesting that tamoxifen activates transcription to promote the differentiation of all cell types in taste buds, rather than activating particular signaling pathways in specific cell types. These findings indicate that tamoxifen rapidly triggers a transcriptional switch from proliferation to differentiation in the circumvallate taste epithelium, highlighting a potential confounding effect in taste research that employs tamoxifen administration. DOI： 10.1038/s41598-025-32701-8 Scopus PubMed

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