J Reconstr Microsurg 2002; 18(6): 495-502
DOI: 10.1055/s-2002-33321
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Peripheral Nerve Regeneration in the Apolipoprotein-E-Deficient Mouse

Eric M. Genden1 , Osamu Watanabe2 , Susan E. Mackinnon2 , Daniel A. Hunter2 , Suzanne R. Strasberg2
  • 1Department of Otolaryngology-Head and Neck Surgery, Mount Sinai School of Medicine, New York, New York
  • 2Department of Surgery, Division of Plastic Surgery, Washington University School of Medicine, St. Louis, MO
Further Information

Publication History

Publication Date:
14 August 2002 (online)

ABSTRACT

Apolipoprotein E (apo E) is thought to mediate the reutilization of myelin cholesterol for nerve regeneration. Prior research suggests that apo E is not essential for nerve regeneration following a nerve crush injury. This study was conducted to determine if apo E is essential for nerve regeneration after nerve transection and interposition nerve autograft. Nerve regeneration of transgenic apo E-deficient mice was compared with control mice after a sciatic nerve neurolysis and repair and interposition autograft. Histomorphometric assessment and histology were performed on distal nerve segments to evaluate nerve regeneration. Apo E-deficient mice demonstrated no difference in total fiber number or nerve fiber width when compared with controls; however, the nerve fiber density and percent neural tissue of apo E-deficient mice were significantly less than controls following nerve repair. Apo E deficiency does not affect nerve regeneration. It is likely that the low nerve fiber density and the low percent neural tissue associated with apo E-deficiency result from impairment in the disposal of myelin debris.

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