Nature Neuroscience6, 863 - 868 (2003)
Published online: 6 July 2003; | doi:10.1038/nn1088
Robust neural integration from retinal transplants in mice deficient in GFAP and vimentin
Reiko Kinouchi1, Masumi Takeda1, 3, Liu Yang1, Ulrika Wilhelmsson2, Andrea Lundkvist2, Milos Pekny2, 4
& Dong Feng Chen1, 4
1
Schepens Eye Research Institute and Department of Ophthalmology, Program in Neuroscience, Harvard Medical School, 20 Staniford Street, Boston, Massachusetts 02114 USA.
2
Department of Medical Biochemistry, Göteborg University, Medicinaregatan 9A, SE-413 90 Göteborg, Sweden.
3
Department of Ophthalmology, Asahikawa Medical College, Midorigaoka-Higashi 2-1-1-1, Asahikawa 078-8510, Japan.
With recent progress in neuroscience and stem-cell research, neural transplantation has emerged as a promising therapy for treating CNS diseases. The success of transplantation has been limited, however, by the restricted ability of neural implants to survive and establish neuronal connections with the host. Little is known about the mechanisms responsible for this failure. Neural implantation triggers reactive gliosis, a process accompanied by upregulation of intermediate filaments in astrocytes and formation of astroglial scar tissue. Here we show that the retinas of adult mice deficient in glial fibrillary acidic protein and vimentin, and consequently lacking intermediate filaments in reactive astrocytes and Müller cells, provide a permissive environment for grafted neurons to migrate and extend neurites. The transplanted cells integrated robustly into the host retina with distinct neuronal identity and appropriate neuronal projections. Our results indicate an essential role for reactive astroglial cells in preventing neural graft integration after transplantation.
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