Reducing Fibrous Encapsulation of Implanted Devices Using Biomaterials

Fibrous encapsulation, commonly referred to as scar formation, can cause failure in many biomedical implants, such as in the artificial pancreas for type I diabetes treatment. Scar tissue prevents wastes and nutrients from being exchanged in the implant, ultimately rendering the treatment painful or ineffective. For example, one potential therapeutic for type I diabetes involves using alginate to protect insulin-producing cells. This artificial pancreas provides diabetics with their much needed insulin on-demand. If scar tissue forms around this artificial pancreas, the device loses the ability to deliver insulin and becomes useless. Our goal is to reduce the fibrous encapsulation of implants using poly-l-arginine-based biomaterials and improve the understanding of how fibroblasts involved in scar formation respond to biomaterials. We show that our materials can reduce fibrous capsule formation by inhibiting the activation of latent transforming growth factor β (L-TGF-β). Active TGF-β leads to capsule formation by activating fibroblasts to differentiate into myofibroblasts, which contract collagen. We also discuss the viability of our biomaterials and presence of VEGF in vitro. This research will not only improve the success of the artificial pancreas, but other biomaterials.