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Sema-3A indirectly disrupts the regeneration process of goldfish optic nerve after controlled injury |
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| Authors: | Shira Rosenzweig Dorit Raz-Prag Anat Nitzan Ronit Galron Ma’ayan Paz Gunnar Jeserich Gera Neufeld Ari Barzilai Arieh S. Solomon |
| Affiliation: | 1. Departments of Neurobiology, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, 69978, Israel 4. Goldschleger Eye Research Institute, Tel Aviv University, Sheba MedicalCenter, Tel Hashomer, Israel 2. Department of Neurobiology, University of Osnabrück, 49069, Osnabrück, Germany 3. Cancer and Vascular Biology Research Center, Rappaport Research Institute in the Medical Sciences, The Bruce Rappaport Faculty of Medicine, Technion, Haifa, 31096, Israel 5. Department of Neurobiochemistry, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, 69978, Israel |
| Abstract: | BackgroundNeurons of adult mammalian CNS are prevented from regenerating injured axons due to formation of a non-permissive environment. The retinal ganglion cells (RGC), which are part of the CNS, share this characteristic. In sharp contrast, the RGC of lower vertebrates, such as fish, are capable of re-growing injured optic nerve axons, and achieve, through a complex multi-factorial process, functional vision after injury. Semaphorin-3A (sema-3A), a member of the class 3 semaphorins known for its repellent and apoptotic activities, has previously been shown to play a key role in the formation of a non-permissive environment after CNS injury in mammalians. |
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