Expression of E- and P-cadherin during tooth morphogenesis and cytodifferentiation of ameloblasts

Abstract

Cell-cell adhesion is fundamental in morphogenesis and is known to be mediated by several groups of cell adhesion molecules. Cadherins are a group of such molecules involved in the Ca2+-dependent cell-cell adhesion mechanism and are found in most kinds of tissue. In this study using indirect immunofluorescence microscopy, we analyzed the distribution of two kinds of cadherins, E- and P-cadherin, in developing tooth germs. In the molar tooth germs at the early bud stage, marginal cells of the epithelial tooth bud expressed both E- and P-cadherin, whereas central cells expressed only E-cadherin. At the cap stage, in addition to the cells of the inner and outer enamel epithelium, which outline the enamal organ, cells of the enamel knot, which is thought to control tooth morphogenesis, strongly expressed P-cadherin. The expression of P-cadherin was prominent in the inner enamel epithelium during the early to mid bell stage, and was also evident in the non-dividing cell masses at future cusp tips, which are the so-called secondary enamel knots. In the tooth germ at the late bell stage when the cells of the inner enamel epithelium began to polarize to differentiate into ameloblasts, the polarizing ameloblasts lost P-cadherin and strongly expressed E-cadherin. However, E-cadherin was also lost from polarized ameloblasts at later stages. The stratum intermedium and the stellate reticulum were E-cadherin positive from the bell stage onward even at the stages when the ameloblasts became E-cadherin negative again. These results suggest that the differential expression of E- and P-cadherin during morphogenetic stages plays a role in the regulation of tooth morphogenesis, whereas alteration of E-cadherin expression during later stages of tooth development is related to differentiation and function of the ameloblasts and other cells supporting amelogenesis.

Differential Expression of the Tight Junction Proteins, Claudin‐1, Claudin‐4, Occludin, ZO‐1, and PAR3, in the Ameloblasts of Rat Upper Incisors

“…The distributions of integral membrane proteins forming intercellular junctions such as occludin, claudins, cadherins, and connexins in ameloblasts have been reported previously (Inai et al, 1997;Obara et al, 1998;Joã o and Arana-Chavez, 2004;Bello et al, 2007;Ohazama and Sharpe, 2007). Early and late differentiating rat ameloblasts at the bell stage expressed claudin-1 at the proximal and distal TJs and also expressed occludin except for the distal TJs of late differentiating ameloblasts (Joã o and Arana-Chavez, 2004).…”

Cooperation of nectin‐1 and nectin‐3 is required for normal ameloblast function and crown shape development in mouse teeth

“…Previous studies revealed that nectin deficiency caused alterations in cellular junctions including adherens, tight and desmosomal junctions (Inagaki et al, 2005;Barron et al, 2008;Takai et al, 2008). During development and enamel formation, SR and SI cells are connected by adherens and desmosomal junctions (Fausser et al, 1998;Obara et al, 1998;Gritli-Linde et al, 2002). Our immunohistological analysis revealed severe reduction in the membrane localization of the adherens junction molecule E-cadherin, as well as of the desmosomal junction component desmoplakin, in the SI of the compound mutants ( Fig.…”

MMP20 Cleaves E-Cadherin and Influences Ameloblast Development

“…2008]. Ameloblasts express E-, N-, and P-cadherins as well as ␤ -catenin and p120-catenin (p120), during dental enamel development [Palacios et al, 1995;Fausser et al, 1998;Obara et al, 1998;Terling et al, 1998;Sorkin et al, 2000;Heymann et al, 2002;Bartlett et al, 2010]. A major pathway for signal transduction by AJs involves the regulation of ␤ -catenin, which can act as either a structural protein at cell-cell junctions or a transcription factor in the cell nucleus [reviewed in Munshi and Stack, 2006].…”