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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Japanese Society for Regenerative Medicine
2016
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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 |
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. |
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