Protective effects of glial cell line-derived neurotrophic factor in ischemic brain injury

Y. Wang, C. F. Chang, M. Morales, Y. H. Chiang, J. Hoffer

研究成果: 雜誌貢獻文章

85 引文 (Scopus)

摘要

Glial cell line-derived neurotrophic factor (GDNF), a member of the transforming growth factor-β (TGF-β) superfamily, has been shown to have trophic activity on dopaminergic neurons. Recent studies indicate that GDNF can protect the cerebral hemispheres from damage induced by middle cerebral arterial ligation. We found that such neuroprotective effects are mediated through specific GDNF receptor alpha-1 (GFRα1). Animals with a deficiency in GFRα-1 have less GDNF-induced neuroprotection. Ischemia also enhances nitric oxide synthase (NOS) activity, which can be attenuated by GDNF. These data suggest that GDNF can protect against ischemic injury through a GFRα-1/NOS mechanism. We also found that the receptor for GDNF, GFRα1, and its signaling moiety c-Ret were upregulated, starting immediately after ischemia. This upregulation suggests that activation of an endogenous neuroprotective mechanism occurs so that responsiveness of GDNF can be enhanced at very early stages during ischemia.

原文英語
頁(從 - 到)423-437
頁數15
期刊Annals of the New York Academy of Sciences
962
出版狀態已發佈 - 2002
對外發佈Yes

指紋

Glial Cell Line-Derived Neurotrophic Factor
Brain Injuries
Brain
Glial Cell Line-Derived Neurotrophic Factor Receptors
Ischemia
Nitric Oxide Synthase
Nerve Growth Factor Receptors
Transforming Growth Factors
Neuroprotective Agents
Dopaminergic Neurons
Cerebrum
Neurons
Brain Injury
Cells
Animals
Ligation
Chemical activation
Up-Regulation
Wounds and Injuries

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

引用此文

Protective effects of glial cell line-derived neurotrophic factor in ischemic brain injury. / Wang, Y.; Chang, C. F.; Morales, M.; Chiang, Y. H.; Hoffer, J.

於: Annals of the New York Academy of Sciences, 卷 962, 2002, p. 423-437.

研究成果: 雜誌貢獻文章

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AU - Hoffer, J.

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N2 - Glial cell line-derived neurotrophic factor (GDNF), a member of the transforming growth factor-β (TGF-β) superfamily, has been shown to have trophic activity on dopaminergic neurons. Recent studies indicate that GDNF can protect the cerebral hemispheres from damage induced by middle cerebral arterial ligation. We found that such neuroprotective effects are mediated through specific GDNF receptor alpha-1 (GFRα1). Animals with a deficiency in GFRα-1 have less GDNF-induced neuroprotection. Ischemia also enhances nitric oxide synthase (NOS) activity, which can be attenuated by GDNF. These data suggest that GDNF can protect against ischemic injury through a GFRα-1/NOS mechanism. We also found that the receptor for GDNF, GFRα1, and its signaling moiety c-Ret were upregulated, starting immediately after ischemia. This upregulation suggests that activation of an endogenous neuroprotective mechanism occurs so that responsiveness of GDNF can be enhanced at very early stages during ischemia.

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