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Migration of lacZ positive cells from the tibialis anterior to the extensor digitorum longus muscle of the X-linked muscular dystrophic (mdx) mouse
Authors:Diana J Watt  Janusz Karasinski  Marjorie A England
Institution:(1) Department of Anatomy, Charing Cross and Westminster Medical School, Fulham Palace Road, W6 8RF London, UK;(2) Department of Cytology and Histology, Institute of Zoology, Jagiellonian University, Karasia 6, Krakow, Poland;(3) Department of Anatomy, University of Leicester, Medical Sciences Building, University Road, LE1 7RH Leicester, UK
Abstract:Summary C2 mouse myogenic cells carrying the lacZ gene coding for beta-galactosidase (beta-gal) were injected into the tibialis anterior muscle of dystrophin-deficient mdx mice. Introduced cells were shown to have been incorporated into fibres of the injected muscle by virtue of the colocalization of beta-gal and dystrophin within them. Synthetic Nuclepore membrane inserted between the injected tibialis anterior and adjacent extensor digitorum longus muscle permitted the visualization of cells migrating between the two muscles through the pores of the membrane. Although the exact nature of the cells passing through the Nuclepore could not be determined by this method, they were thought to include implanted myogenic cells. Evidence for this was gained by the presence of beta-gal/dystrophin positive fibres within the extensor digitorum longus. Incorporation of cells into the adjacent extensor digitorum longus was greater in animals where this muscle had been autografted by the cutting and resuturing of the distal tendon. Autografted extensor digitorum longi differed from those which had not been subject to this procedure, by undergoing extensive fibre degeneration followed by regeneration, and further by the stripping of their surrounding epimysial covering. Implanted cells substantially participated in extensor digitorum longus fibre formation in these mice, up to 31% of their fibres 3 weeks after implantation coexpressing both the introduced lacZ gene product and the dystrophin gene product, the latter not normally expressed within the fibres of this myopathic recipient.
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