Sandor B, Fintor K, Felszeghy Sz, Juhasz T, Reglodi D, Mark L, Kiss P, Jungling A, Fulop B D, Nagy A D, Hashimoto H, Zakany R, Nagy A, Tamas A
Department of Dentistry, Oral and Maxillofacial Surgery, Medical School, University of Pecs, Pecs, Hungary.
J Mol Neurosci. 2014 Nov;54(3):331-41. doi: 10.1007/s12031-014-0392-6. Epub 2014 Aug 12.
Pituitary adenylate cyclase activating polypeptide (PACAP) is a pleiotropic neuropeptide with widespread distribution. It plays pivotal role in neuronal development. PACAP-immunoreactive fibers have been found in the tooth pulp, and recently, it has been shown that PACAP may also play a role in the regeneration of the periodontium after luxation injuries. However, there is no data about the effect of endogenous PACAP on tooth development. Ectodermal organogenesis including tooth development is regulated by different members of bone morphogenetic protein (BMP), fibroblast growth factor (FGF), hedgehog (HH), and Wnt families. There is also a growing evidence to support the hypothesis that PACAP interacts with sonic hedgehog (SHH) receptor (PTCH1) and its downstream target (Gli1) suggesting its role in tooth development. Therefore, our aim was to study molar tooth development in mice lacking endogenous PACAP. In this study morphometric, immunohistochemical and structural comparison of molar teeth in pre-eruptive developmental stage was performed on histological sections of 7-day-old wild-type and PACAP-deficient mice. Further structural analysis was carried out with Raman microscope. The morphometric comparison of the 7-day-old samples revealed that the dentin was significantly thinner in the molars of PACAP-deficient mice compared to wild-type animals. Raman spectra of the enamel in wild-type mice demonstrated higher diversity in secondary structure of enamel proteins. In the dentin of PACAP-deficient mice higher intracrystalline disordering in the hydroxyapatite molecular structure was found. We also obtained altered SHH, PTCH1 and Gli1 expression level in secretory ameloblasts of PACAP-deficient mice compared to wild-type littermates suggesting that PACAP might play an important role in molar tooth development and matrix mineralization involving influence on SHH signaling cascade.
垂体腺苷酸环化酶激活多肽(PACAP)是一种多效性神经肽,分布广泛。它在神经元发育中起关键作用。牙髓中已发现有PACAP免疫反应性纤维,最近研究表明,PACAP在牙脱位损伤后牙周组织的再生中也可能发挥作用。然而,关于内源性PACAP对牙齿发育影响的数据尚无报道。包括牙齿发育在内的外胚层器官发生受骨形态发生蛋白(BMP)、成纤维细胞生长因子(FGF)、刺猬蛋白(HH)和Wnt家族不同成员的调节。也有越来越多的证据支持这样的假说,即PACAP与音猬因子(SHH)受体(PTCH1)及其下游靶点(Gli1)相互作用,提示其在牙齿发育中的作用。因此,我们的目的是研究缺乏内源性PACAP的小鼠磨牙的发育情况。在本研究中,对7日龄野生型和PACAP缺陷型小鼠的组织学切片进行了磨牙萌出前发育阶段的形态计量学、免疫组织化学和结构比较。使用拉曼显微镜进行了进一步的结构分析。7日龄样本的形态计量学比较显示,与野生型动物相比,PACAP缺陷型小鼠磨牙中的牙本质明显更薄。野生型小鼠牙釉质的拉曼光谱显示牙釉质蛋白二级结构的多样性更高。在PACAP缺陷型小鼠的牙本质中,发现羟基磷灰石分子结构的晶体内无序程度更高。与野生型同窝小鼠相比,我们还发现PACAP缺陷型小鼠分泌性成釉细胞中SHH、PTCH1和Gli1的表达水平发生了改变,这表明PACAP可能在磨牙发育和基质矿化中起重要作用,涉及对SHH信号级联的影响。