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Influence of insulin‐like growth factor‐I (IGF‐I) on nerve autografts and tissue‐engineered nerve grafts
Author(s) -
Fansa Hisham,
Schneider Wolfgang,
Wolf Gerald,
Keilhoff Gerburg
Publication year - 2002
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.10165
Subject(s) - basal lamina , regeneration (biology) , axon , sciatic nerve , insulin like growth factor , schwann cell , medicine , nerve guidance conduit , epineurial repair , growth factor , anatomy , nerve growth factor , biology , microbiology and biotechnology , ultrastructure , receptor
To overcome the problems of limited donor nerves for nerve reconstruction, we established nerve grafts made from cultured Schwann cells and basal lamina from acellular muscle and used them to bridge a 2‐cm defect of the rat sciatic nerve. Due to their basal lamina and to viable Schwann cells, these grafts allow regeneration that is comparable to autologous nerve grafts. In order to enhance regeneration, insulin‐like growth factor (IGF‐I) was locally applied via osmotic pumps. Autologous nerve grafts with and without IGF‐I served as controls. Muscle weight ratio was significantly increased in the autograft group treated with IGF‐I compared to the group with no treatment; no effect was evident in the tissue‐engineered grafts. Autografts with IGF‐I application revealed a significantly increased axon count and an improved g‐ratio as indicator for “maturity” of axons compared to autografts without IGF‐I. IGF‐I application to the engineered grafts resulted in a decreased axon count compared to grafts without IGF‐I. The g‐ratio, however, revealed no significant difference between the groups. Local administration of IGF‐I improves axonal regeneration in regular nerve grafts, but not in tissue‐engineered grafts. Seemingly, in these grafts the interactive feedback mechanisms of neuron, glial cell, and extracellular matrix are not established, and IGF‐I cannot exert its action as a pleiotrophic signal. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 87‐93, 2002