Glucose-Dependent Insulin Secretion from β Cell Spheroids Is Enhanced by Embedding into Softer Alginate Hydrogels Functionalised with RGD Peptide.
Md Lutful AminKylie DengHien A TranReena SinghJelena Rnjak-KovacinaPeter ThornPublished in: Bioengineering (Basel, Switzerland) (2022)
Type 1 diabetes results from the loss of pancreatic β cells, reduced insulin secretion and dysregulated blood glucose levels. Replacement of these lost β cells with stem cell-derived β cells, and protecting these cells within macro-device implants is a promising approach to restore glucose homeostasis. However, to achieve this goal of restoration of glucose balance requires work to optimise β cell function within implants. We know that native β cell function is enhanced by cell-cell and cell-extracellular matrix interactions within the islets of Langerhans. Reproducing these interactions in 2D, such as culture on matrix proteins, does enhance insulin secretion. However, the impact of matrix proteins on the 3D organoids that would be in implants has not been widely studied. Here, we use native β cells that are dispersed from islets and reaggregated into small spheroids. We show these β cell spheroids have enhanced glucose-dependent insulin secretion when embedded into softer alginate hydrogels conjugated with RGD peptide (a common motif in extracellular matrix proteins). Embedding into alginate-RGD causes activation of integrin responses and repositioning of liprin, a protein that controls insulin secretion. We conclude that insulin secretion from β cell spheroids can be enhanced through manipulation of the surrounding environment.
Keyphrases
- extracellular matrix
- induced apoptosis
- blood glucose
- single cell
- type diabetes
- cell cycle arrest
- cell therapy
- drug delivery
- signaling pathway
- stem cells
- endoplasmic reticulum stress
- mesenchymal stem cells
- cardiovascular disease
- insulin resistance
- adipose tissue
- photodynamic therapy
- skeletal muscle
- weight loss
- tissue engineering
- small molecule
- binding protein