The Experts below are selected from a list of 2028 Experts worldwide ranked by ideXlab platform
Takashi Saku - One of the best experts on this subject based on the ideXlab platform.
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Reciprocal expressions between α-dystroglycan and integrin β1, perlecan receptors, in the murine Enamel Organ development.
Gene Expression Patterns, 2013Co-Authors: Hiroko Ida-yonemochi, Hayato Ohshima, Hidemitsu Harada, Takashi SakuAbstract:Signals of perlecan, an extracellular matrix molecule, which accumulates within the intercellular spaces of the stellate reticulum of the Enamel Organ, are mediated by at least two receptors, dystroglycan (DG) and integrin β1, in a case-dependent manner in various events in embryogenesis and pathogenesis. This study aims to understand the expression profiles of these two perlecan receptors at both protein and gene levels in murine Enamel Organ development. Before birth, α-DG was immunolocalized in stellate reticulum cells, in which perlecan was colocalized, while integrin β1 was mainly distributed in the peripheral Enamel Organ cells as well as the dental mesenchymal cells. On and after postnatal Day 1, the expression of α-DG was dramatically decreased in the stellate reticulum, while integrin β1 was enhanced around blood vessels within the Enamel Organ. Furthermore, biosyntheses of α-DG and integrin β1 by dental epithelial and pulp mesenchymal cells were confirmed in vitro by using immunofluorescence and reverse-transcriptase polymerase chain reaction. The results suggest that DG is a perlecan receptor that specifically functions in the stellate reticulum of the embryonic stage, but that dental epithelial and mesenchymal cells are maturated by capturing perlecan signals differentially through integrin β1.
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morphogenetic roles of perlecan in the tooth Enamel Organ an analysis of overexpression using transgenic mice
Matrix Biology, 2011Co-Authors: Hiroko Idayonemochi, Yoshihiko Yamada, Ichiro Satokata, Hayato Ohshima, Toshiya Sato, Minesuke Yokoyama, Takashi SakuAbstract:Perlecan, a heparan sulfate proteoglycan, is enriched in the intercellular space of the Enamel Organ. To understand the role of perlecan in tooth morphogenesis, we used a keratin 5 promoter to generate transgenic (Tg) mice that over-express perlecan in epithelial cells, and examined their tooth germs at tissue and cellular levels. Immunohistochemistry showed that perlecan was more strongly expressed in the Enamel Organ cells of Tg mice than in wild-type mice. Histopathology showed wider intercellular spaces in the stellate reticulum of the Tg molars and loss of cellular polarity in the Enamel Organ, especially in its cervical region. Hertwig's epithelial root sheath (HERS) cells in Tg mice were irregularly aligned due to excessive deposits of perlecan along the inner, as well as on the outer sides of the HERS. Tg molars had dull-ended crowns and outward-curved tooth roots and their Enamel was poorly crystallized, resulting in pronounced attrition of molar cusp areas. In Tg mice, expression of integrin β1 mRNA was remarkably higher at E18, while expression of bFGF, TGF-β1, DSPP and Shh was more elevated at P1. The overexpression of perlecan in the Enamel Organ resulted in irregular morphology of teeth, suggesting that the expression of perlecan regulates growth factor signaling in a stage-dependent manner during each step of the interaction between ameloblast-lineage cells and mesenchymal cells.
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Heparanase, heparan sulfate and perlecan distribution along with the vascular penetration during stellate reticulum retraction in the mouse Enamel Organ.
Archives of Oral Biology, 2010Co-Authors: Hiroko Ida-yonemochi, Motowo Nakajima, Takashi SakuAbstract:Abstract Objective Immunohistochemical and gene expression profiles of heparanase were determined in murine molar tooth germs from their embryonic to postnatal stages, paying special attention to neovascularization within the Enamel Organ, which is poorly vascularized before birth. Design Protein and gene expression profiles of heparanase, heparan sulfate (HS), vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), and perlecan were comparatively examined by immunohistochemistry and in-situ hybridization, respectively, in mouse mandibular molar tooth germs from embryonic day 11.5 to postnatal day 6. At the same time, their mRNA expression levels were also confirmed by reverse transcriptase-polymerase chain reaction using laser-captured microdissection of Enamel Organ tissues. Results Stellate reticulum cells highly expressed perlecan but only slightly expressed heparanase and HS in their embryonic days. On and after postnatal day 1, the expressions of heparanase became dramatically higher in the stellate reticulum, while HS disappeared leaving the immunopositivity for perlecan core protein. Immunohistochemically, HS was enhanced around blood vessels which were newly formed after birth within the Enamel Organs, whose volume was also regressive. Similar expression patterns were obtained for VEGF and TGF-β1. Conclusions Such synchronized expression modes among the HS metabolism-related molecules suggested that heparanase plays an important role in degradation of HS chains, which is closely related to vascular penetration into the stellate reticulum, which may be one of the driving forces for the postnatal regression of the Enamel Organ.
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Perlecan, a basement membrane-type heparan sulfate proteoglycan, in the Enamel Organ: its intraepithelial localization in the stellate reticulum.
Journal of Histochemistry & Cytochemistry, 2005Co-Authors: Hiroko Ida-yonemochi, Kazufumi Ohshiro, Wael Swelam, Hamdy Metwaly, Takashi SakuAbstract:SUMMARY The localization and biosynthesis of perlecan, a basement membrane–type heparan sulfate proteoglycan, were studied in developing tooth germs by using murine molars in neonatal and postnatal stages and primary cultured cells of the Enamel Organ and dental papilla to demonstrate the role of perlecan in normal odontogenesis. Perlecan was immunolocalized mainly in the intercellular spaces of the Enamel Organ as well as in the dental papilla/pulp or in the dental follicle. By in situ hybridization, mRNA signals for perlecan core protein were intensely demonstrated in the cytoplasm of stellate reticulum cells and in dental papilla/pulp cells, including odontoblasts and fibroblastic cells in the dental follicle. Furthermore, the in vitro biosyntheses of perlecan core protein by the Enamel Organ and dental papilla/pulp cells were confirmed by immunofluorescence, immunoprecipitation, and reverse transcriptase–polymerase chain reaction. The results indicate that perlecan is synthesized by the dental epithelial cells and is accumulated in their intercellular spaces to form the characteristic stellate reticulum, whose function is still unknown. (J Histochem Cytochem 53:763–772, 2005)
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immunolocalization of cd44 and heparan sulfate chains on the stratum intermedium and papillary layer in the rat Enamel Organ
Archives of Histology and Cytology, 1995Co-Authors: Hiroaki Nakamura, Shinichi Kenmotsu, Takashi Saku, Shin Kimura, Hideo Sakai, Hidehiro OzawaAbstract:We studied the immunohistochemical localization of CD44 and heparan sulfate (HS) chains in rat Enamel Organ by confocal laser scanning microscopy and transmission electron microscopy. We also investigated the binding sites of basic fibroblast growth factor (bFGF), one of the heparin-binding growth factors (HBGF), on Microslicer-sections to clarify its role in the cell-cell interaction of HS.At the differentiation stage of ameloblasts, weak immunoreactivity for CD44 was detected on the plasma membrane of the inner Enamel epithelium, external Enamel epithelium and the cells adjacent to the inner Enamel epithelium. In accordance with the differentiation of preameloblasts into secretory ameloblasts, this immunoreactivity increased in stratum intermedium cells. At the secretory stage, stratum intermedium cells showed the most intense immunoreactivity in the Enamel Organ. At the maturation stage, strong immunoreactiviry was seen on papillary layer cells. On the other hand, the lateral plasma membrane of ruffleended (RA) and smooth-ended ameloblast (SA) showed weak reactivity. No immunoreactivity was detected on the ruffled border of RA and the distal plasma membrane of SA. Immunolocalization of HS chains was similar to that of CD44. The binding activity of bFGF was also intense on stratum intermedium cells and papillary layer cells.These findings suggest that: 1) stratum intermedium cells and papillary layer cells express CD44 and HS chains in accordance with their differentiation; 2) HS chains on the plasma membrane of these cells may regulate calcium transport by their negative charge; and 3) HS chains on the stratum intermedium and papillary layer may play an important role in the differentiation and activity of ameloblasts by preserving HBGF.
Hiroko Ida-yonemochi - One of the best experts on this subject based on the ideXlab platform.
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Role of perlecan, a basement membrane-type heparan sulfate proteoglycan, in Enamel Organ morphogenesis
Journal of Oral Biosciences, 2013Co-Authors: Hiroko Ida-yonemochiAbstract:Abstract Perlecan is a multifunctional heparan sulfate proteoglycan that controls cell-signaling events by interacting with several growth factors, cytokines, and other signaling molecules. Perlecan was thought to be localized only in the basement membrane, but recently, intraepithelial localization of perlecan has been demonstrated in some pathophysiological situations. Therefore, perlecan is expected to modulate epithelial cell behavior. Our recent study demonstrated that perlecan accumulates in the stellate reticulum of the Enamel Organ of murine molar tooth germs in a stage-specific manner. To understand the function of perlecan in the Enamel Organ, we generated transgenic ( Tg ) mice that overexpressed perlecan in epithelial cells by using the keratin 5 promoter. Perlecan Tg molars had dull-ended crowns and outward-curved tooth roots, and their Enamel was poorly crystallized. The constant overexpression of perlecan and the accompanying disOrganized distribution of perlecan-related molecules in the Enamel Organ resulted in irregular tooth morphology. These results indicate that the time schedule of intraepithelial perlecan expression appears to be critically controlled during Enamel Organ development. In this brief review, we have described the dynamics of perlecan and its receptors and the timing of cleavage of heparan sulfate chains in odontogenesis, focusing on Enamel Organ development, and discussed the role of perlecan in Enamel Organ morphogenesis.
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Reciprocal expressions between α-dystroglycan and integrin β1, perlecan receptors, in the murine Enamel Organ development.
Gene Expression Patterns, 2013Co-Authors: Hiroko Ida-yonemochi, Hayato Ohshima, Hidemitsu Harada, Takashi SakuAbstract:Signals of perlecan, an extracellular matrix molecule, which accumulates within the intercellular spaces of the stellate reticulum of the Enamel Organ, are mediated by at least two receptors, dystroglycan (DG) and integrin β1, in a case-dependent manner in various events in embryogenesis and pathogenesis. This study aims to understand the expression profiles of these two perlecan receptors at both protein and gene levels in murine Enamel Organ development. Before birth, α-DG was immunolocalized in stellate reticulum cells, in which perlecan was colocalized, while integrin β1 was mainly distributed in the peripheral Enamel Organ cells as well as the dental mesenchymal cells. On and after postnatal Day 1, the expression of α-DG was dramatically decreased in the stellate reticulum, while integrin β1 was enhanced around blood vessels within the Enamel Organ. Furthermore, biosyntheses of α-DG and integrin β1 by dental epithelial and pulp mesenchymal cells were confirmed in vitro by using immunofluorescence and reverse-transcriptase polymerase chain reaction. The results suggest that DG is a perlecan receptor that specifically functions in the stellate reticulum of the embryonic stage, but that dental epithelial and mesenchymal cells are maturated by capturing perlecan signals differentially through integrin β1.
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Heparanase, heparan sulfate and perlecan distribution along with the vascular penetration during stellate reticulum retraction in the mouse Enamel Organ.
Archives of Oral Biology, 2010Co-Authors: Hiroko Ida-yonemochi, Motowo Nakajima, Takashi SakuAbstract:Abstract Objective Immunohistochemical and gene expression profiles of heparanase were determined in murine molar tooth germs from their embryonic to postnatal stages, paying special attention to neovascularization within the Enamel Organ, which is poorly vascularized before birth. Design Protein and gene expression profiles of heparanase, heparan sulfate (HS), vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), and perlecan were comparatively examined by immunohistochemistry and in-situ hybridization, respectively, in mouse mandibular molar tooth germs from embryonic day 11.5 to postnatal day 6. At the same time, their mRNA expression levels were also confirmed by reverse transcriptase-polymerase chain reaction using laser-captured microdissection of Enamel Organ tissues. Results Stellate reticulum cells highly expressed perlecan but only slightly expressed heparanase and HS in their embryonic days. On and after postnatal day 1, the expressions of heparanase became dramatically higher in the stellate reticulum, while HS disappeared leaving the immunopositivity for perlecan core protein. Immunohistochemically, HS was enhanced around blood vessels which were newly formed after birth within the Enamel Organs, whose volume was also regressive. Similar expression patterns were obtained for VEGF and TGF-β1. Conclusions Such synchronized expression modes among the HS metabolism-related molecules suggested that heparanase plays an important role in degradation of HS chains, which is closely related to vascular penetration into the stellate reticulum, which may be one of the driving forces for the postnatal regression of the Enamel Organ.
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Perlecan, a basement membrane-type heparan sulfate proteoglycan, in the Enamel Organ: its intraepithelial localization in the stellate reticulum.
Journal of Histochemistry & Cytochemistry, 2005Co-Authors: Hiroko Ida-yonemochi, Kazufumi Ohshiro, Wael Swelam, Hamdy Metwaly, Takashi SakuAbstract:SUMMARY The localization and biosynthesis of perlecan, a basement membrane–type heparan sulfate proteoglycan, were studied in developing tooth germs by using murine molars in neonatal and postnatal stages and primary cultured cells of the Enamel Organ and dental papilla to demonstrate the role of perlecan in normal odontogenesis. Perlecan was immunolocalized mainly in the intercellular spaces of the Enamel Organ as well as in the dental papilla/pulp or in the dental follicle. By in situ hybridization, mRNA signals for perlecan core protein were intensely demonstrated in the cytoplasm of stellate reticulum cells and in dental papilla/pulp cells, including odontoblasts and fibroblastic cells in the dental follicle. Furthermore, the in vitro biosyntheses of perlecan core protein by the Enamel Organ and dental papilla/pulp cells were confirmed by immunofluorescence, immunoprecipitation, and reverse transcriptase–polymerase chain reaction. The results indicate that perlecan is synthesized by the dental epithelial cells and is accumulated in their intercellular spaces to form the characteristic stellate reticulum, whose function is still unknown. (J Histochem Cytochem 53:763–772, 2005)
Hayato Ohshima - One of the best experts on this subject based on the ideXlab platform.
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msx2 prevents stratified squamous epithelium formation in the Enamel Organ
Journal of Dental Research, 2018Co-Authors: M. Nakatomi, Chihiro Nakatomi, Shinichi Kenmotsu, R.l. Maas, Hiroko Idayonemochi, Kotaro Saito, Hayato OhshimaAbstract:Tooth Enamel is manufactured by the inner Enamel epithelium of the multilayered Enamel Organ. Msx2 loss-of-function mutation in a mouse model causes an abnormal accumulation of epithelial cells in ...
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msx2 prevents stratified squamous epithelium formation in the Enamel Organ
Journal of Dental Research, 2018Co-Authors: M. Nakatomi, Chihiro Nakatomi, Shinichi Kenmotsu, R.l. Maas, Hiroko Idayonemochi, Kotaro Saito, Hayato OhshimaAbstract:Tooth Enamel is manufactured by the inner Enamel epithelium of the multilayered Enamel Organ. Msx2 loss-of-function mutation in a mouse model causes an abnormal accumulation of epithelial cells in the Enamel Organ, but the underlying mechanism by which Msx2 regulates amelogenesis is poorly understood. We therefore performed detailed histological and molecular analyses of Msx2 null mice. Msx2 null ameloblasts and stratum intermedium (SI) cells differentiated normally in the early stages of amelogenesis. However, during subsequent developmental stages, the outer Enamel epithelium (OEE) became highly proliferative and transformed into a keratinized stratified squamous epithelium that ectopically expressed stratified squamous epithelium markers, including Heat shock protein 25, Loricrin, and Keratin 10. Moreover, expression of hair follicle-specific keratin genes such as Keratin 26 and Keratin 73 was upregulated in the Enamel Organ of Msx2 mutants. With the accumulation of keratin in the stellate reticulum (SR) region and subsequent odontogenic cyst formation, SI cells gradually lost the ability to differentiate, and the expression of Sox2 and Notch1 was downregulated, leading to ameloblast depolarization. As a consequence, the Organization of the Msx2 mutant Enamel Organ became disturbed and Enamel failed to form in the normal location. Instead, there was ectopic mineralization that likely occurred within the SR. In summary, we show that during amelogenesis, Msx2 executes a bipartite function, repressing the transformation of OEE into a keratinized stratified squamous epithelium while simultaneously promoting the development of a properly differentiated Enamel Organ competent for Enamel formation.
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Reciprocal expressions between α-dystroglycan and integrin β1, perlecan receptors, in the murine Enamel Organ development.
Gene Expression Patterns, 2013Co-Authors: Hiroko Ida-yonemochi, Hayato Ohshima, Hidemitsu Harada, Takashi SakuAbstract:Signals of perlecan, an extracellular matrix molecule, which accumulates within the intercellular spaces of the stellate reticulum of the Enamel Organ, are mediated by at least two receptors, dystroglycan (DG) and integrin β1, in a case-dependent manner in various events in embryogenesis and pathogenesis. This study aims to understand the expression profiles of these two perlecan receptors at both protein and gene levels in murine Enamel Organ development. Before birth, α-DG was immunolocalized in stellate reticulum cells, in which perlecan was colocalized, while integrin β1 was mainly distributed in the peripheral Enamel Organ cells as well as the dental mesenchymal cells. On and after postnatal Day 1, the expression of α-DG was dramatically decreased in the stellate reticulum, while integrin β1 was enhanced around blood vessels within the Enamel Organ. Furthermore, biosyntheses of α-DG and integrin β1 by dental epithelial and pulp mesenchymal cells were confirmed in vitro by using immunofluorescence and reverse-transcriptase polymerase chain reaction. The results suggest that DG is a perlecan receptor that specifically functions in the stellate reticulum of the embryonic stage, but that dental epithelial and mesenchymal cells are maturated by capturing perlecan signals differentially through integrin β1.
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morphogenetic roles of perlecan in the tooth Enamel Organ an analysis of overexpression using transgenic mice
Matrix Biology, 2011Co-Authors: Hiroko Idayonemochi, Yoshihiko Yamada, Ichiro Satokata, Hayato Ohshima, Toshiya Sato, Minesuke Yokoyama, Takashi SakuAbstract:Perlecan, a heparan sulfate proteoglycan, is enriched in the intercellular space of the Enamel Organ. To understand the role of perlecan in tooth morphogenesis, we used a keratin 5 promoter to generate transgenic (Tg) mice that over-express perlecan in epithelial cells, and examined their tooth germs at tissue and cellular levels. Immunohistochemistry showed that perlecan was more strongly expressed in the Enamel Organ cells of Tg mice than in wild-type mice. Histopathology showed wider intercellular spaces in the stellate reticulum of the Tg molars and loss of cellular polarity in the Enamel Organ, especially in its cervical region. Hertwig's epithelial root sheath (HERS) cells in Tg mice were irregularly aligned due to excessive deposits of perlecan along the inner, as well as on the outer sides of the HERS. Tg molars had dull-ended crowns and outward-curved tooth roots and their Enamel was poorly crystallized, resulting in pronounced attrition of molar cusp areas. In Tg mice, expression of integrin β1 mRNA was remarkably higher at E18, while expression of bFGF, TGF-β1, DSPP and Shh was more elevated at P1. The overexpression of perlecan in the Enamel Organ resulted in irregular morphology of teeth, suggesting that the expression of perlecan regulates growth factor signaling in a stage-dependent manner during each step of the interaction between ameloblast-lineage cells and mesenchymal cells.
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transient expression of heat shock protein hsp 25 in the dental pulp and Enamel Organ during odontogenesis in the rat incisor
Archives of Histology and Cytology, 2000Co-Authors: Hayato Ohshima, Yoshiro Kawano, Satoshi Wakisaka, Hisao Ajima, Kayoko Nozawainoue, Takeyasu MaedaAbstract:The expression of heat shock protein (Hsp) 25 during odontogenesis in the dental pulp and Enamel Organ of rat incisors was investigated by immunocytochemistry and confocal microscopy. In the process of dentin formation, immature odontoblasts first exhibited Hsp 25-immunoreactivity, and increased in immunointensity with the advance of their differentiation. In the dental pulp, in contrast, intense immunoreaction in the mesenchymal cells became weak or negative in parallel with the progress of cell differentiation. The immunoreaction for Hsp 25 in the Enamel Organ revealed a characteristic stage-related alteration during amelogenesis. In secretory ameloblasts, the immunoreaction for Hsp 25 was found throughout their cell bodies, intense reactivity being located near the proximal and distal terminal webs. At the maturation stage, ruffle-ended ameloblasts (RA) consistently showed Hsp 25-immunoreactivity throughout the cell bodies, whereas smooth-ended ameloblasts (SA) lacking a ruffled border were weak in immunoreaction at the distal cytoplasm. Other cellular elements of the Enamel Organ were negative. The subcellular localization of Hsp 25-immunoreactivity in this study appeared essentially identical to that of actin filaments as demonstrated by confocal microscopy using rhodamine-labeled phalloidin. These inununocytochemical data suggest that the Hsp 25 molecule is involved in reinforcement of the cell layer following cell movement during odontogenesis and in the formation and maintenance of the ruffled border of RA.
Jeremy J Mao - One of the best experts on this subject based on the ideXlab platform.
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mtor plays a pivotal role in multiple processes of Enamel Organ development principally through the mtorc1 pathway and in part via regulating cytoskeleton dynamics
Developmental Biology, 2020Co-Authors: Jinxuan Zheng, Xuguang Nie, Michael Cruciger, Peixin Yang, Jeremy J MaoAbstract:We herein report that deletion of mTOR in dental epithelia caused defective development of multiple cell layers of the Enamel Organ, which culminated in tooth malformation and cystogenesis. Specifically, cells of the stellate reticulum and stratum intermedium were poorly formed, resulting in cystic changes. The pre-ameloblasts failed to elongate along the apical-basal axis and persisted vigorous expression of Sox2 and P63, which are normally downregulated during cytodifferentiation. Expression of amelogenic markers was also attenuated in mutants. Cell proliferation and cell sizes in mutants were significantly reduced over time. Importantly, we found reduced amounts and aberrant aggregations of cytoskeletal components in mutants, along with attenuated expression of cytoskeleton regulator Cdc42, whose epithelial deletion causes a similar phenotype. Moreover, disruption of actin assembly in an Organ culture system affected cell proliferation and cytodifferentiation of tooth germs, supporting a causative role of mTOR-regulated cytoskeleton dynamics for the observed phenotype of mTOR mutant mice. In further support of this view, we showed that mTOR overactivation caused increased cytoskeletal component synthesis and assembly, along with accelerated cytodifferentiation in the Enamel Organ. Finally, we demonstrated that mTOR regulated Enamel Organ development principally through the mTORC1 pathway.
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epithelial cdc42 deletion induced Enamel Organ defects and cystogenesis
Journal of Dental Research, 2018Co-Authors: J Zheng, X Nie, A J Yoon, Xin Zhang, M Vats, L Xiang, Z Tian, Jeremy J MaoAbstract:Cdc42, a Rho family small GTPase, regulates cytoskeleton Organization, vesicle trafficking, and other cellular processes in development and homeostasis. However, Cdc42's roles in prenatal tooth development remain elusive. Here, we investigated Cdc42 functions in mouse Enamel Organ. Cdc42 showed highly dynamic temporospatial patterns in the developing Enamel Organ, with robust expression in the outer Enamel epithelium, stellate reticulum (SR), and stratum intermedium layers. Strikingly, epithelium-specific Cdc42 deletion resulted in cystic lesions in the Enamel Organ. Cystic lesions were first noted at embryonic day 15.5 and progressively enlarged during gestation. At birth, cystic lesions occupied the bulk of the entire Enamel Organ, with intracystic erythrocyte accumulation. Ameloblast differentiation was retarded upon epithelial Cdc42 deletion. Apoptosis occurred in the Cdc42 mutant Enamel Organ prior to and synchronously with cystogenesis. Transmission electron microscopy examination showed disrupted actin assemblies, aberrant desmosomes, and significantly fewer cell junctions in the SR cells of Cdc42 mutants than littermate controls. Autophagosomes were present in the SR cells of Cdc42 mutants relative to the virtual absence of autophagosome in the SR cells of littermate controls. Epithelium-specific Cdc42 deletion attenuated Wnt/β-catenin and Shh signaling in dental epithelium and induced aberrant Sox2 expression in the secondary Enamel knot. These findings suggest that excessive cell death and disrupted cell-cell connections may be among multiple factors responsible for the observed cystic lesions in Cdc42 mutant Enamel Organs. Taken together, Cdc42 exerts multidimensional and pivotal roles in Enamel Organ development and is particularly required for cell survival and tooth morphogenesis.
Thomas G H Diekwisch - One of the best experts on this subject based on the ideXlab platform.
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daughters of the Enamel Organ development fate and function of the stratum intermedium stellate reticulum and outer Enamel epithelium
Stem Cells and Development, 2016Co-Authors: Hui Liu, Xiulin Yan, Mirali Pandya, Xianghong Luan, Thomas G H DiekwischAbstract:The tooth Enamel Organ (EO) is a complex epithelial cell assembly involved in multiple aspects of tooth development, including amelogenesis. The present study focuses on the role of the nonameloblast layers of the EO, the stratum intermedium, the stellate reticulum, and the outer Enamel epithelium (OEE). The secretory stage stratum intermedium was distinguished by p63-positive epithelial stem cell marks, highly specific alkaline phosphatase labeling, as well as multiple desmosomes and gap junctions. At the location of the presecretory stage stellate reticulum, the pre-eruption EO prominently featured the papillary layer (PL) as a keratin immunopositive network of epithelial strands between tooth crowns and oral epithelium. PL cell strands contained numerous p63-positive epithelial stem cells, while BrdU proliferative cells were detected at the outer boundaries of the PL, suggesting that the stellate reticulum/PL epithelial cell sheath proliferated to facilitate an epithelial seal during tooth eruption. Comparative histology studies demonstrated continuity between the OEE and the general lamina of continuous tooth replacement in reptiles, and the outer layer of Hertwig's epithelial root sheath in humans, implicating the OEE as the formative layer for continuous tooth replacement and tooth root extension. Cell fate studies in Organ culture verified that the cervical portion of the mouse molar EO gave rise to Malassez rest-like cell islands. Together, these studies indicate that the nonameloblast layers of the EO play multiple roles during odontogenesis, including the maintenance of several p63-positive stem cell reservoirs, a role during tooth root morphogenesis and tooth succession, a stabilizing function for the ameloblast layer, the facilitation of ion transport from the EO capillaries to the Enamel layer, as well as safe and seamless tooth eruption.