The effect of molecular weights of microencapsulating polymers on viability of mouse-cloned pancreatic β-cells: biomaterials, osmotic forces and potential applications in diabetes treatment

Abstract

Introduction: Ideal cell-containing microcapsules should be capable of maintaining cell viability and exhibit significant structural stability to support cellular functionality. To date, such microcapsules remain unavailable; thus, this study used our well-established microencapsulating methods to examine a total of 32 different microencapsulating formulations and correlate polymers’ molecular weights (M_wt) and UDCA addition, with cell viability and microcapsules’ stability, postmicroencapsulation.

Methods: MIN6 mouse-cloned pancreatic β-cells were microencapsulated using control (n = 16; without UDCA) and test (n = 16; with UDCA) different polymers. Confocal microscopic imaging, cell viability, and microcapsules’ stability were assessed.

Results: Best cell viability (>50%) was obtained at average M_wt of 50,000 g/mol (poly-l-ornithine), followed by 110,000 g/mol (poly-l-lysine). There was no linear correlation between M_wt and viability. Confocal imagining showed similar microcapsules’ shape and cell distribution among all different polymers’ molecular weights, which suggests that the microencapsulating method was efficient and maintained microcapsules’ uniformity. UDCA addition resulted in enhanced osmotic stability of the microcapsules and improved cell viability, when the formulation contained 1% polylornithine, 1% polyethylene glycol, 20% Eudragit^® NM30D, 1% polytetrafluoroethylene, or 5% pentamethylcyclopentasiloxane.

Conclusions: UDCA addition improved microenvironmental conditions within the microcapsules but this effect was largely dependent on the polymer systems used.

Keywords:

• Artificial cell microencapsulation
• MIN6
• diabetes mellitus
• biomaterials
• polymer

Acknowledgements

The authors acknowledge Australian Postgraduate Award (APA) + Curtin Research Scholarship (CRS) for their support. The authors also acknowledge the Curtin University Microscopy and Microanalysis Facility (MMF) for access to equipment. The authors also acknowledge the Curtin Health Innovation Research Institute (CHIRI) for provision of laboratory space and technology platforms utilized in this study. Min6 cells were kindly provided by Dr. Jun-ichi Miyazaki. Grant Morahan and Emma Jamieson are supported by funds from the National Health and Medical Research Council Program grant (NHMRC1037321 M) and Diabetes Research WA. Ryu Takechi is supported by funds from Alzheimer’s Australia Dementia Research Foundation, Australian National Health and Medical Research Council and WA Department of Health.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

Grant Morahan and Emma Jamieson are supported by funds from the National Health and Medical Research Council Program grant (NHMRC1037321 M) and Diabetes Research WA. Ryu Takechi is supported by funds from Alzheimer’s Australia Dementia Research Foundation, Australian National Health and Medical Research Council and WA Department of Health.