These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Differential expression profiles between α-dystroglycan and integrin β1 in ameloblastoma: two possible perlecan signalling pathways for cellular growth and differentiation.
    Author: Ida-Yonemochi H, Ahsan MS, Saku T.
    Journal: Histopathology; 2011 Jan; 58(2):234-45. PubMed ID: 21255062.
    Abstract:
    AIMS: Intercellular deposition of perlecan, an extracellular matrix molecule, results in characteristic stellate reticulum-like structures in ameloblastomas. The aims of this study were to elucidate which types of perlecan receptors function within any particular type of tissue architecture of ameloblastoma. METHODS AND RESULTS: Protein and gene expression profiles for α-dystroglycan and integrin β1 were examined comparatively with those of their ligands in ameloblastoma using surgical specimens and cells in primary culture. In the follicular-type tumour cell foci, α-dystroglycan was localized uniformly over the stellate reticulum-like cells, while integrin β1 was restricted mainly to peripheral cells facing the stroma with the interface of the basement membrane, which was also rich in perlecan. In the plexiform-type, mRNA and protein signals for α-dystroglycan were enhanced in the periphery of tumour cell foci, especially in their invading fronts. Integrin β1 was also immunolocalized in the basal cell zone, which was considered to be the proliferation centre of ameloblastoma cells. Furthermore, biosynthesis of α-dystroglycan and integrin β1 by ameloblastoma cells was confirmed in vitro using immunofluorescence and reverse transcriptase-polymerase chain reaction. CONCLUSIONS: Ameloblastoma cells proliferate and are differentiated by capturing perlecan differentially with α-dystroglycan and integrin β1, respectively.
    [Abstract] [Full Text] [Related] [New Search]