Endocytotic functions of ameloblasts and odontoblasts: Immunocytochemical and tracer studies on the uptake of plasma proteins

Nanci, Antonio; Fortin, Myriam; Ghitescu, Lucian

doi:10.1002/(sici)1097-0185(199606)245:2<219::aid-ar9>3.0.co;2-r

Cited by 33 publications

(29 citation statements)

References 62 publications

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“…The fact remains, however, that after 30 years of intensive research, observations reported in the original paper on ameloblast resorptive activity still remain to be confirmed unequivocally (Reith and Cotty, 1967). Investigators have shown reasonably conclusively that both ameloblasts and papillary layer cells can actively uptake small amounts (pinocytosis) and/or large amounts (endocytosis) of any protein tracer that gains access to the intercellular spaces of the enamel organ or apical membranes of ameloblasts (Skobe and Garant, 1974;Kallenbach, 1980;Ozawa, 1980, 1984;Crenshaw and Takano, 1982;Sasaki et al, , 1984aSasaki, 1984b;Takano, 1995;Nanci et al, 1996a). These proteins will move into endosomes and then into lysosomes of all enamel organ cells, Figure 10.…”

Section: Endocytosis and Pinocytosismentioning

confidence: 98%

“…where they are degraded Garant, 1974, Smith, 1979;Kallenbach, 1980, Takano and Ozawa, 1980, 1984Crenshaw and Takano, 1982;, 1984a, Sasaki, 1984bSalama et al, 1989bSalama et al, , 1990aSalama et al, , 1991Takano, 1995;Nanci et al, 1996a). This does not prove, however, that aged enamel matrix proteins are exiting the enamel and are naturally present at these sites.…”

Section: Endocytosis and Pinocytosismentioning

confidence: 99%

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Cellular and Chemical Events During Enamel Maturation

Smith

1998

Critical Reviews in Oral Biology & Medicine

637

836

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This review focuses on the process of enamel maturation, a series of events associated with slow, progressive growth in the width and thickness of apatitic crystals. This developmental step causes gradual physical hardening and transformation of soft, newly formed enamel into one of the most durable mineralized tissues produced biologically. Enamel is the secretory product of specialized epithelial cells, the ameloblasts, which make this covering on the crowns of teeth in two steps. First, they roughly "map out" the location and limits (overall thickness) of the entire extracellular layer as a protein-rich, acellular, and avascular matrix filled with thin, ribbon-like crystals of carbonated hydroxyapatite. These initial crystals are organized spatially into rod and interrod territories as they form, and rod crystals are lengthened by Tomes' processes in tandem with appositional movement of ameloblasts away from the dentin surface. Once the full thickness of enamel has been formed, ameloblasts initiate a series of repetitive morphological changes at the enamel surface in which tight junctions and deep membrane infoldings periodically appear (ruffle-ended), then disappear for short intervals (smooth-ended), from the apical ends of the cells. As this happens, the enamel covered by these cells changes rhythmically in net pH from mildly acidic (ruffle-ended) to near-physiologic (smooth-ended) as mineral crystals slowly expand into the "spaces" (volume) formerly occupied by matrix proteins and water. Matrix proteins are processed and degraded by proteinases throughout amelogenesis, but they undergo more rapid destruction once ameloblast modulation begins. Ruffle-ended ameloblasts appear to function primarily as a regulatory and transport epithelium for controlling the movement of calcium and other ions such as bicarbonate into enamel to maintain buffering capacity and driving forces optimized for surface crystal growth. The reason ruffle-ended ameloblasts become smooth-ended periodically is unknown, although this event seems to be crucial for sustaining long-term crystal growth.

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Section: Endocytosis and Pinocytosismentioning

confidence: 98%

Section: Endocytosis and Pinocytosismentioning

confidence: 99%

Cellular and Chemical Events During Enamel Maturation

Smith

1998

Critical Reviews in Oral Biology & Medicine

637

836

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“…However, if a mechanism for enamel matrix protein removal involves a significant uptake of partially degraded proteins (i.e. where the epitopes are recognizable), and their subsequent trafficking to late endosomes and lysosomes, then the presumption must be that ameloblasts absorb secreted proteins (and the debris of these secreted proteins) during amelogenesis [41][42][43][44]. This type of resorption would then be described more as a receptor-mediated endocytosis.…”

Section: Introductionmentioning

confidence: 99%

Cellular uptake of amelogenin, and its localization to CD63, and Lamp1-positive vesicles

Shapiro

Wen

Okamoto

et al. 2006

Cell. Mol. Life Sci.

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Proteins of the developing enamel matrix include amelogenin, ameloblastin and enamelin. Of these three proteins amelogenin predominates. Protein-protein interactions are likely to occur at the ameloblast Tomes' processes between membrane-bound proteins and secreted enamel matrix proteins. Such protein-protein interactions could be associated with cell signaling or endocytosis. CD63 and Lamp1 are ubiquitously expressed, are lysosomal integral membrane proteins, and localize to the plasma membrane. CD63 and Lamp1 interact with amelogenin in vitro. In this study our objective was to study the molecular events of intercellular trafficking of an exogenous source of amelogenin, and related this movement to the spatiotemporal expression of CD63 and Lamp1 using various cell lineages. Exogenously added amelogenin moves rapidly into the cell into established Lamp1-positive vesicles that subsequently localize to the perinuclear region. These data indicate a possible mechanism by which amelogenin, or degraded amelogenin peptides, are removed from the extracellular matrix during enamel formation and maturation.

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“…The fetuin-gold complex (particles of ‫51ف‬ nm in diameter; 25 g/ml) was purchased from EY Laboratories (San Mateo, CA). Bovine serum albumin (Sigma) was tagged with dinitrophenol (DNP) using the method of Little and Eisen (1967), as reported previously (Ghitescu and Bendayan 1993;Nanci et al 1996a). …”

Section: Administration Of Tracersmentioning

confidence: 99%

In Vivo Model for the Experimental Manipulation of Calcified Tissues: A Surgical Approach for Accessing the Odontogenic Organ and Associated Tissues of the Rat Incisor

Daniel

Nanci

1999

J Histochem Cytochem.

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SUMMARYThe tooth organ is extensively used in developmental biology to investigate organogenesis and cell differentiation. It also represents an advantageous system for the study of the various cellular and extracellular matrix events that regulate the formation of both collagenous and noncollagenous calcified tissues. This article describes an in vivo surgical approach to access and experimentally manipulate the tooth organ and supporting tissues of the rat incisor. By use of a dental drill, a "window" was created through the alveolar bone on the buccal aspect of the hemimandible at the apical end of the incisor. It is at this site that epithelial and mesenchymal precursors are situated and undergo cellular differentiation to give rise to cells of the odontogenic organ. Active bone remodeling is also observed in this area to accommodate posterior growth of the tooth. An osmotic minipump connected to the bony window through an outlet catheter was used for controlled and continuous administration of experimental agents over a predetermined period of time. To validate the model, vinblastine sulfate, fetuin-gold, and dinitrophenylated albumin were thus infused. The animals were then sacrificed and the hemimandibles were processed for histological and immunocytochemical analyses. The effects of the drug and the presence of tracers were restricted to the treated hemimandible and were found in the enamel organ and pulp, as well as in the tooth supporting tissues. Cellular changes typically associated with the administration of vinblastine were obtained, and tracers were localized both in the extracellular milieu and within the endosomal/lysosomal elements of cells. These results suggest that this new surgical approach could serve as an advantageous in vivo model in which various chemical agents, therapeutic drugs, molecular probes are locally administered to study the molecular events that regulate calcified tissue formation.

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Endocytotic functions of ameloblasts and odontoblasts: Immunocytochemical and tracer studies on the uptake of plasma proteins

Cited by 33 publications

References 62 publications

Cellular and Chemical Events During Enamel Maturation

Cellular and Chemical Events During Enamel Maturation

Cellular uptake of amelogenin, and its localization to CD63, and Lamp1-positive vesicles

In Vivo Model for the Experimental Manipulation of Calcified Tissues: A Surgical Approach for Accessing the Odontogenic Organ and Associated Tissues of the Rat Incisor

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