Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Acknowledgments
- Part I Special lectures
- Part II Oxidative stress
- Part III Apoptosis
- Part IV Hot topics
- Part V Hemorrhage, edema and secondary injury
- Part VI Inflammation
- Part VII Gene transfer and therapy
- 22 Adenoviral vectors for gene therapy in stroke
- 23 Gene transfer of glial cell line-derived neurotrophic factor prevents ischemic brain injury
- 24 Vasomotor effects of nitric oxide, superoxide dismutases and calcitonin gene-related peptide
- Part VIII Neurogenesis and plasticity
- Part IX Magnetic resonance imaging in clinical stroke
- Part X Risk factors, clinical trials and new therapeutic horizons
- Index
- Plate section
23 - Gene transfer of glial cell line-derived neurotrophic factor prevents ischemic brain injury
from Part VII - Gene transfer and therapy
Published online by Cambridge University Press: 02 November 2009
- Frontmatter
- Contents
- List of contributors
- Preface
- Acknowledgments
- Part I Special lectures
- Part II Oxidative stress
- Part III Apoptosis
- Part IV Hot topics
- Part V Hemorrhage, edema and secondary injury
- Part VI Inflammation
- Part VII Gene transfer and therapy
- 22 Adenoviral vectors for gene therapy in stroke
- 23 Gene transfer of glial cell line-derived neurotrophic factor prevents ischemic brain injury
- 24 Vasomotor effects of nitric oxide, superoxide dismutases and calcitonin gene-related peptide
- Part VIII Neurogenesis and plasticity
- Part IX Magnetic resonance imaging in clinical stroke
- Part X Risk factors, clinical trials and new therapeutic horizons
- Index
- Plate section
Summary
Topical application of glial cell line-derived neurotrophic factor reduces ischemic brain injury after permanent middle cerebral artery occlusion in rats
Glial cell line-derived neurotrophic factor (GDNF), a member of the transforming growth factor-β (TGF-β) superfamily, plays important roles not only in the differentiation of neurons during normal development, but also in the survival and recovery of many populations of mature neurons. It has been reported that GDNF has protective effects on various injuries of the central and peripheral nervous systems in vitro and in vivo. However, a possible protective effect of GDNF in focal cerebral ischemia, and the exact mechanism of the ameliorative effect of GDNF in brain ischemic injury are not fully understood.
Caspase-1 (interleukin-1β converting enzyme (ICE)), caspase-2 and caspase-3 have been thought to play important roles in ischemic neuronal injury. Expression or upregulation of caspase mRNAs have been reported in some ischemic injury models. Inhibition of caspase family proteases reduced ischemic and excitotoxic neuronal damage, and expression of a dominant negative mutant of ICE or a mutant ICE inhibitory protein in transgenic mice prevented or attenuated ischemic brain injury. Therefore, the progression of ischemic neuronal injuries may be greatly associated with activation of these caspases through an apoptotic process. However, it has been uncertain whether caspases are also induced during, or involved in, neuronal death after permanent middle cerebral artery occlusion (MCAO).
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- Chapter
- Information
- Cerebrovascular Disease22nd Princeton Conference, pp. 269 - 283Publisher: Cambridge University PressPrint publication year: 2002