Importance of Cell-Matrix Interactions in Rat Islet Beta-Cell Secretion In Vitro: Role of a6B1 Integrin

Bosco D., Meda P., Halban P.A, Rouiller D.G.

Diabetes, 2000

The present work addresses the influence of short-term cell-matrix interactions on islet beta-cell function and provides the first insight into the molecular basis of these interactions. When primary rat beta-cells were allowed to attach to a laminin-332 rich matrix (804G matrix), there was an increased insulin secretory response to secretagogues. This change was the result of an increase in the proportion of actively secreting beta-cells and in the amount of insulin secreted per active cell. In turn, the spreading or flattening of beta-cells on this matrix was enhanced by secretagogues, and flattened cells secreted more insulin than rounded cells. a6B1 integrins are present heterogeneous at the surface of islet cells in situ and is upregulated by insulin secretagogues. a6B1 expression is higher in spreading cells and anti-a6B1–specific antibodies decrease spreading. These observations demonstrate that islet cell-matrix interactions can improve the sensitivity of insulin cells to glucose and are mediated, at least in part, by a6B1 integrins, suggesting that outside-in signaling through a6B1 integrin plays a major role in the regulation of B-cell function.

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