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Title: Expression of TGF-beta receptors I and II in the human dental pulp by in situ hybridization. Author: Sloan AJ, Couble ML, Bleicher F, Magloire H, Smith AJ, Farges JC. Journal: Adv Dent Res; 2001 Aug; 15():63-7. PubMed ID: 12640743. Abstract: Members of the TGF-beta family of growth factors are important in modulation of odontoblast secretory activity during dental tissue repair. Odontoblast expression of TGF-beta isoforms during development leads to their sequestration within the dentin matrix, from where they may be released during carious injury and participate in reparative processes. Two receptors, implicated in TGF-beta-mediated cell signaling, have been identified immunohistochemically in both odontoblasts and pulpal cells of healthy and carious human molar teeth. This study aimed to characterize the expression of the TGF-beta receptors I and II in sound and carious teeth by means of in situ hybridization, to help our understanding of the response of these cells to TGF-beta stimulation. Sound and carious human third molar teeth were routinely processed immediately following extraction, and 10-microns paraffin-embedded sections prepared. These sections were hybridized with 32P-labeled probes to TGF-beta receptors I and II, and the subsequent signal was detected by autoradiography. mRNA for both receptors I and II was mainly detected within the odontoblasts and nerve-associated cells of healthy tissues, with expression at lower levels seen within the subodontoblast and pulp core cells. The expression in odontoblasts was higher for TGF-beta receptor I than for receptor II. Expression of both receptors was more homogenous in all pulp cells within carious teeth, because of an increase of signal within the underlying pulp cell population, including blood-vessel-associated cells. We conclude that the TGF-beta receptors I and II were expressed in odontoblasts and pulp cells, and that subtle variations in the levels of their expression could be involved in the tissue response to injury.[Abstract] [Full Text] [Related] [New Search]