超氧化物歧化酶3在缺氧诱导的小鼠磨牙发育缺陷中的可能作用。

IF 2.6 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Journal of Oral Biosciences Pub Date : 2025-01-01 DOI:10.1016/j.job.2024.100611

Yeming Lu, Yukiho Kobayashi, Yuki Niki, Keiji Moriyama

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引用次数: 0

摘要

目的：探讨缺氧对小鼠牙胚发育的影响及其机制。方法：从E14.5小鼠胚胎中提取牙胚，分为对照组和缺氧组进行器官培养。缺氧组小鼠缺氧（0%氧）3 h，再缺氧21 h。2 d或7 d后，采集标本进行形态计量学分析、逆转录-定量聚合酶链反应、免疫组化（IHC）和免疫荧光染色（IF）。此外，采用免疫组化方法分析了超氧化物歧化酶3 （SOD3）在C57BL/6小鼠下颌磨牙胚中的表达规律。SOD抑制剂N， N-二乙基二硫代氨基甲酸钠(DETC；400 μM)常温下处理3 d，然后进行形态测定、免疫组化和IF。结果：缺氧组与对照组相比，缺氧组牙齿尺寸明显减小，牙尖明显减少，细胞增殖减少，上皮细胞凋亡增加。对照组Sod3 mRNA表达高于其他Sod家族成员表达。缺氧组Sod3 mRNA和Sod3蛋白表达显著降低，缺氧诱导因子-1表达和活性氧水平升高。SOD3主要在E12.5 ~ E17.5牙上皮中表达。DETC损害了对照组的牙胚发育，导致与缺氧组相似的表型，并显著降低了上皮中amelogenin和msh homeobox 2的表达。结论：缺氧影响牙胚发育。SOD3可能在这一过程中起到保护作用。

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Possible role of superoxide dismutase 3 in hypoxia-induced developmental defects in murine molars

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Possible role of superoxide dismutase 3 in hypoxia-induced developmental defects in murine molars

Objectives

To investigate the effects of hypoxia on tooth germ development in mice and explore the underlying mechanisms.

Methods

Tooth germs were extracted from E14.5 mouse embryos and divided into the control and hypoxia groups for organ culture. The hypoxia group was exposed to hypoxia (0% oxygen) for 3 h, followed by normoxia for 21 h. After 2 or 7 days, samples were collected for morphometric analysis, reverse transcription-quantitative polymerase chain reaction, immunohistochemistry (IHC), and immunofluorescent staining (IF). Additionally, superoxide dismutase 3 (SOD3) expression patterns in mandibular molar tooth germs from C57BL/6 mouse embryos were analyzed using IHC. The SOD inhibitor sodium N, N-diethyldithiocarbamate trihydrate (DETC; 400 μM) was applied under normoxia for 3 days, followed by morphometry, IHC, and IF.

Results

After 7 days, the hypoxia group exhibited significantly smaller tooth size, fewer cusps, reduced cell proliferation, and increased apoptosis in the epithelium compared to the control group. Sod3 mRNA expression was higher than other Sod family member expressions in the control group. In the hypoxia group, Sod3 mRNA and SOD3 protein expression were significantly decreased, whereas hypoxia-inducible factor-1 expression and reactive oxygen species levels were increased. SOD3 was primarily expressed in the dental epithelium from E12.5 to E17.5. DETC impaired tooth germ development in the control group, resulting in a phenotype similar to that of the hypoxia group, and significantly reduced amelogenin and msh homeobox 2 expression in the epithelium.