Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, United States.
Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, United States.
Matrix Biol. 2022 Jan;105:72-86. doi: 10.1016/j.matbio.2021.11.002. Epub 2021 Nov 20.
Studies on animal models with mutations in ameloblastin gene have suggested that the extracellular matrix protein ameloblastin (AMBN) plays important roles in controlling cell-matrix adhesion and ameloblast polarization during amelogenesis. In order to examine the function of AMBN in cell polarization and morphology, we developed an in vitro 3D cell culture model to examine the effect of AMBN and amelogenin (AMEL) addition on ameloblast cell lines. We further used high resolution confocal microscopy to detect expression of polarization markers in response to AMBN addition. Addition of AMBN to the 3D culture matrix resulted in the clustering and elongation (higher aspect ratio) of ALC in a dose dependent manner. The molar concentration of AMEL required to exact this response from ALC was 2.75- times greater than that of AMBN. This polarization effect of ameloblastin was attributable directly to an evolutionary conserved domain within its exon 5-encoded region. The lack of exon 6-encoded region also influenced AMBN-cell interactions but to a lesser extent. The clusters formed with AMBN were polarized with expression of E-cadherin, Par3 and Cldn1 assembly at the nascent cell-cell junctions. The elongation effect was specific to epithelial cells of ameloblastic lineage ALC and LS8 cells. Our data suggest that AMBN may play critical signaling roles in the initiation of cell polarity by acting as a communicator between cell-cell and cell-matrix interactions. Our investigation has important implications for understanding the function of ameloblastin in enamel-cell matrix adhesion and the outcomes may contribute to efforts to develop strategies for enamel tissue regeneration.
研究表明,釉原蛋白基因突变的动物模型中的细胞外基质蛋白釉原蛋白(AMBN)在控制釉质发生过程中的细胞-基质黏附和釉柱细胞极性方面发挥着重要作用。为了研究 AMBN 在细胞极性和形态中的功能,我们开发了一种体外 3D 细胞培养模型,以研究 AMBN 和釉原蛋白(AMEL)添加对釉柱细胞系的影响。我们进一步使用高分辨率共聚焦显微镜检测 AMBN 添加后极化标记物的表达。AMBN 添加到 3D 培养基质中会导致 ALC 聚集和伸长(更高的纵横比),呈剂量依赖性。ALC 对 AMBN 产生这种反应所需的 AMEL 摩尔浓度是 AMBN 的 2.75 倍。AMBN 的这种极化作用归因于其外显子 5 编码区域内的进化保守结构域。缺乏外显子 6 编码区域也会影响 AMBN-细胞相互作用,但影响较小。用 AMBN 形成的簇具有极化特性,在新形成的细胞-细胞连接处表达 E-钙黏蛋白、Par3 和 Cldn1 组装。伸长效应是釉柱细胞系 ALC 和 LS8 细胞上皮细胞所特有的。我们的数据表明,AMBN 可能通过充当细胞-细胞和细胞-基质相互作用之间的通讯器,在细胞极性的起始中发挥关键的信号作用。我们的研究对于理解 AMBN 在釉质细胞基质黏附中的功能具有重要意义,其结果可能有助于开发釉质组织再生策略的努力。