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Controlling the Release of Neurotrophin‐3 and Chondroitinase ABC Enhances the Efficacy of Nerve Guidance Conduits
Author(s) -
Donsante Anthony,
Xue Jiajia,
Poth Kelly M.,
Hardcastle Nathan S.,
Diniz Bruna,
O'Connor Deirdre M.,
Xia Younan,
Boulis Nicholas M.
Publication year - 2020
Publication title -
advanced healthcare materials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.288
H-Index - 90
eISSN - 2192-2659
pISSN - 2192-2640
DOI - 10.1002/adhm.202000200
Subject(s) - axon , neurotrophin , sciatic nerve , nerve guidance conduit , compound muscle action potential , chemistry , controlled release , biophysics , biomedical engineering , materials science , anatomy , medicine , nanotechnology , biology , biochemistry , electrophysiology , receptor
Nerve guidance conduits (NGCs) have the potential to replace autografts in repairing peripheral nerve injuries, but their efficacy still needs to be improved. The efficacy of NGCs is augmented by neurotrophic factors that promote axon growth and by enzymes capable of degrading molecules that inhibit axon growth. In the current study, two types of NGCs loaded with factors (both neurotrophin‐3 and chondroitinase ABC) are constructed and their abilities to repair an 8 mm gap in the rat sciatic nerve are examined. The factors are encapsulated in microparticles made of a phase‐change material (PCM) or collagen and then sandwiched between two layers of electrospun fibers. The use of PCM allows to achieve pulsed release of the factors upon irradiation with a near‐infrared laser. The use of collagen enables slow, continuous release via diffusion. The efficacy is evaluated by measuring compound muscle action potentials (CMAP) in the gastrocnemius muscle and analyzing the nerve histology. Continuous release of the factors from collagen results in enhanced CMAP amplitude and increased axon counts in the distal nerve relative to the plain conduit. In contrast, pulsed release of the same factors from PCM shows a markedly adverse impact on the efficacy, possibly by inhibiting axon growth.