Reduction of Cortical Infarction and Impairment of Apoptosis in NGF-Transgenic Mice Subjected to Permanent Focal Ischemia
| Autor: | Christelle Guégan, Mansouria Merad-Boudia, Yaeko Makiura, Brigitte Sola, Irène Ceballos-Picot, Brigitte Onteniente |
|---|---|
| Přispěvatelé: | Neurodégénérescence : modèles et stratégies thérapeutiques, Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Neuroplasticité et thérapeutique, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Immunité de l'infection et transplantations, Normandie Université (NU)-Normandie Université (NU) |
| Jazyk: | angličtina |
| Rok vydání: | 1998 |
| Předmět: |
Genetically modified mouse
Male medicine.medical_specialty Transgene Recombinant Fusion Proteins [SDV]Life Sciences [q-bio] Central nervous system Ischemia Mice Transgenic Nerve Tissue Proteins Apoptosis Permanent focal ischemia DNA Fragmentation Biology Neuroprotection Brain Ischemia 03 medical and health sciences Cellular and Molecular Neuroscience Mice 0302 clinical medicine Transgenic mouse Internal medicine medicine Animals Nerve Growth Factors Transgenes Promoter Regions Genetic Molecular Biology 030304 developmental biology 0303 health sciences Cerebral Infarction medicine.disease Endocrinology Nerve growth factor medicine.anatomical_structure Reperfusion Injury biology.protein Neurotrophin Neuroscience Proto-Oncogene Proteins c-fos 030217 neurology & neurosurgery Brain infarction |
| Zdroj: | Brain research. Molecular brain research Brain research. Molecular brain research, 1998, 55 (1), pp.133-140. ⟨10.1016/s0169-328x(97)00372-0⟩ |
| DOI: | 10.1016/s0169-328x(97)00372-0⟩ |
| Popis: | International audience; The neuroprotective potential of the nerve growth factor (NGF) against permanent ischemic brain damage has been investigated in vivo using NGF-transgenic (tg) mice. The expression of the transgene is driven by part of the promoter of the proto-oncogene c-fos, which belongs to the first set of genes activated after brain ischemic insult. Wild-type (wt) mice and tg mice were subjected to permanent focal ischemia induced by electrocoagulation of the middle cerebral artery. Twenty four hours (h) after the ischemic shock, when compared to wt, tg mice displayed a 40% reduction of the infarcted area, which lasted up to 1 week. However, infarcted brain areas were similar in wt and tg mice within the first hours post-occlusion, indicating that NGF acted to block the progression of neuronal damage. Kinetics of NGF synthesis assessed by ELISA was in good agreement with the observed neuroprotective effect, since NGF content peaked 6 h post-ischemia. This was further correlated with the time-course of c-Fos immunoreactivity, detectable only from 6 h post-ischemia. The neuroprotective effect of NGF involved the impairment of apoptotic cell death, as evidenced by a marked decrease of the number of apoptotic profiles inside the ischemic zone in tg mice. These results underline the potential of c-fos-NGF-tg mice to study in vivo the molecular and cellular mechanisms of the NGF-induced neuroprotective effect against ischemic damage. |
| Databáze: | OpenAIRE |
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