| First Author | Ida-Yonemochi H | Year | 2011 |
| Journal | Histopathology | Volume | 58 |
| Issue | 2 | Pages | 234-45 |
| PubMed ID | 21255062 | Mgi Jnum | J:226159 |
| Mgi Id | MGI:5696117 | Doi | 10.1111/j.1365-2559.2010.03732.x |
| Citation | Ida-Yonemochi H, et al. (2011) Differential expression profiles between alpha-dystroglycan and integrin beta1 in ameloblastoma: two possible perlecan signalling pathways for cellular growth and differentiation. Histopathology 58(2):234-45 |
| abstractText | 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 alpha-dystroglycan and integrin beta1 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, alpha-dystroglycan was localized uniformly over the stellate reticulum-like cells, while integrin beta1 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 alpha-dystroglycan were enhanced in the periphery of tumour cell foci, especially in their invading fronts. Integrin beta1 was also immunolocalized in the basal cell zone, which was considered to be the proliferation centre of ameloblastoma cells. Furthermore, biosynthesis of alpha-dystroglycan and integrin beta1 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 alpha-dystroglycan and integrin beta1, respectively. |
