Spontaneous Development of Dental Dysplasia in Aged Parp-1 Knockout Mice

Spontaneous Development of Dental Dysplasia in Aged Parp-1 Knockout Mice
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DOI：
10.3390/cells8101157
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发表时间：
2019-10-01
期刊：
CELLS
影响因子：
6
通讯作者：
Masutani, Mitsuko
Masutani, Mitsuko
中科院分区：
生物学2区
文献类型：
--
作者：
Fujihara, Hisako;Nozaki, Tadashige;Masutani, Mitsuko

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聚(ADP-核糖)聚合酶(PARP)-1利用NAD(+)催化多聚ADP-核糖化，参与DNA损伤反应、基因组稳定性和转录。在这项研究中，我们证明了老年PARP-1(-/-)小鼠切牙在ICR/129Sv混合背景和C57BL/6品系中表现出比老年PARP-1(+/+)门牙更频繁的牙齿发育不良，这表明PARP-1缺乏可能参与了老年牙齿发育不良的发展。计算机断层扫描图像证实，在PARP-1(-/-)小鼠中观察到牙齿发育不良的发生率显著更高。PARP-1(-/-)门牙的相对钙化水平在牙釉质和牙本质中均较高(p&lt；0.05)。免疫组织化学结果显示：(1)PARP-1在PARP-1(+/+)切牙的成釉细胞和成牙本质细胞中呈阳性表达，(2)PARP-1(-/-)切牙的牙本质中有弱阳性表达，(3)在PARP-1(-/-)切牙的牙本质中，骨涎蛋白呈阳性表达，提示PARP-1(-/-)切牙牙本质中存在异位成骨。这些结果表明，PARP-1缺乏促进了老年人切牙的牙源性失败。PARP-1缺乏不影响小鼠发育过程中牙本质的发生，提示PARP-1在发育过程中不是牙本质发生所必需的，但可能参与了老年人切牙持续牙本质发生的调节。
Poly(ADP-ribose) polymerase (Parp)-1 catalyzes polyADP-ribosylation using NAD(+) and is involved in the DNA damage response, genome stability, and transcription. In this study, we demonstrated that aged Parp-1(-/-) mouse incisors showed more frequent dental dysplasia in both ICR/129Sv mixed background and C57BL/6 strain compared to aged Parp-1(+/+) incisors, suggesting that Parp-1 deficiency could be involved in development of dental dysplasia at an advanced age. Computed tomography images confirmed that dental dysplasia was observed at significantly higher incidences in Parp-1(-/-) mice. The relative calcification levels of Parp-1(-/-) incisors were higher in both enamel and dentin (p < 0.05). Immunohistochemical analysis revealed (1) Parp-1 positivity in ameloblasts and odontoblasts in Parp-1(+/+) incisor, (2) weaker dentin sialoprotein positivity in dentin of Parp-1(-/-) incisor, and (3) bone sialoprotein positivity in dentin of Parp-1(-/-) incisor, suggesting ectopic osteogenic formation in dentin of Parp-1(-/-) incisor. These results indicate that Parp-1 deficiency promotes odontogenic failure in incisors at an advanced age. Parp-1 deficiency did not affect dentinogenesis during the development of mice, suggesting that Parp-1 is not essential in dentinogenesis during development but is possibly involved in the regulation of continuous dentinogenesis in the incisors at an advanced age.