TAT-Bcl-x(L) improves survival of neuronal precursor cells in the lesioned striatum after focal cerebral ischemia

Autor: Mimount El Aanbouri, Gunnar P.H. Dietz, Mathias Bähr, Thorsten R. Doeppner, Otto W. Witte, Jens Weise, Joachim Gerber
Rok vydání: 2008
Předmět:
Doublecortin Domain Proteins
Male
Striatum
Brain Ischemia
Mice
0302 clinical medicine
0303 health sciences
biology
Cell Death
Stem Cells
Neurogenesis
Cerebral ischemia
Neuroprotection
medicine.anatomical_structure
Neuroprotective Agents
Neurology
Gene Products
tat
Microtubule-Associated Proteins
medicine.medical_specialty
Programmed cell death
Doublecortin Protein
Cell Survival
Recombinant Fusion Proteins
Ischemia
bcl-X Protein
Subventricular zone
Motor Activity
Endogenous neurogenesis
lcsh:RC321-571
03 medical and health sciences
Internal medicine
medicine
Animals
Learning
lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry
030304 developmental biology
business.industry
Dentate gyrus
Neuropeptides
medicine.disease
Corpus Striatum
Doublecortin
Mice
Inbred C57BL
Endocrinology
TAT fusion proteins
nervous system
Space Perception
biology.protein
business
Neuroscience
030217 neurology & neurosurgery
Zdroj: Neurobiology of Disease, Vol 34, Iss 1, Pp 87-94 (2009)
ISSN: 1095-953X
Popis: Cerebral ischemia activates endogenous neurogenesis in the subventricular zone (SVZ) and the dentate gyrus. Consecutively, SVZ-derived neural precursors migrate towards ischemic lesions. However, functional relevance of activated neurogenesis is limited by poor survival of new-born precursors. We therefore employed the HI-virus-derived fusion protein TAT-Bcl-x L to study the effects of acute anti-apoptotic treatment on endogenous neurogenesis and functional outcome after transient cerebral ischemia in mice. TAT-Bcl-x L treatment led to significantly reduced acute ischemic cell death (128 ± 23 vs. 305 ± 65 TUNEL + cells/mm 2 in controls) and infarct volumes resulting in less motor deficits and improved spatial learning. It significantly increased survival of doublecortin (Dcx)-positive neuronal precursors (389 ± 96 vs. 213 ± 97 Dcx + cells in controls) but did not enhance overall post-ischemic cell proliferation or lesion-specific neuronal differentiation 28 days after ischemia. Our data demonstrate that post-stroke TAT-Bcl-x L -treatment results in acute neuroprotection, improved functional outcome, and enhanced survival of lesion-specific neuronal precursor cells after cerebral ischemia in mice.
Databáze: OpenAIRE
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