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β-Galactoside-mediated tissue organization during islet reconstitution

We have previously reported that multi-cellular heteroaggregates comprising murine pancreatic α (αTC1.6) and β (MIN6-m9) cell lines spontaneously acquired islet-like architecture and displayed higher insulin secretion rates. However, the mechanisms of self-organization remain unclear. The objective...

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Detalles Bibliográficos
Autores principales: Kamitori, Sae, Ozeki, Yasuhiro, Kojima, Nobuhiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Japanese Society for Regenerative Medicine 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581812/
https://www.ncbi.nlm.nih.gov/pubmed/31245467
http://dx.doi.org/10.1016/j.reth.2016.01.006
Descripción
Sumario:We have previously reported that multi-cellular heteroaggregates comprising murine pancreatic α (αTC1.6) and β (MIN6-m9) cell lines spontaneously acquired islet-like architecture and displayed higher insulin secretion rates. However, the mechanisms of self-organization remain unclear. The objective of this study is to examine the possibility that a sugar chain participates in the mutual recognition of the cells during reconstitution of the islet-like structure in vitro. Using a lectin-binding assay, we identified Erythrina cristagalli agglutinin (ECA), which particularly recognizes the β-galactoside structure on the surfaces of MIN6-m9 cells. The self-organization of αTC1.6 and MIN6-m9 was obstructed using ECA-bound MIN6-m9 cells. Lactose neutralized the ECA's inhibitory effect on the autonomous rearrangement of αTC1.6 and MIN6-m9 cells, indicating that the inhibition of cell arrangement by ECA was mediated via β-galactoside. We concluded that a β-galactoside sugar chain was central to the reconstitution of the pancreatic islet-like architecture in vitro.