TRANSFORMING GROWTH FACTOR-βS IN NEURODEGENERATIVE DISEASE
Abstract
Transforming growth factors-betas (TGF-betas), a family of multifunctional peptide growth factors, affect cells of the central nervous system (CNS). The three mammalian TGF-beta isoforms, TGF-betas 1, 2 and 3, are expressed in adult human brain. Since neuronal degeneration is a defining feature of CNS degenerative diseases, TGF-beta may be important because it can influence neuronal survival. In vitro TGF-beta promotes survival of rat spinal cord motoneurons and dopaminergic neurons. In addition to direct effects on neuronal survival, TGF-beta treatment of cultured astrocytes induces a reactive phenotype. Thus, TGF-beta may also normalize the extracellular matrix environment in degenerative diseases. The expression of TGF-betas change in response to neuronal injury. TGF-beta 1 expression increases in astrocytes and microglia in animal models of cerebral ischemia, while TGF-beta 2 expression increases in activated astroglial cells in human neurodegenerative diseases. TGF-betas protect neurons from a variety of insults. TGF-beta maintains survival of chick telencephalic neurons made hypoxic by treatment with cyanide and decreases the area of infarction when administered in animal models of cerebral ischemia. In vitro TGF-beta protects neurons from damage induced by treatment with beta-amyloid peptide, FeSO4 (induces production of reactive oxygen species), Ca2+ ionophores, glutamate, glutamate receptor agonists and MPTP (toxic for dopaminergic neurons). TGF-beta maintains mitoch…
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TGF-β1 exerts a protective effect against various neuronal insults.
“Numerous studies have demonstrated that TGF-β1 exerts a protective effect against various neuronal insults46.”
From Identification of a unique TGF-β–dependent molecular and functional signature in microglia (2014) · cites this paper as [46]
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- Authors
- FLANDERS, K.
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 1998-01
- Volume
- 54
- Issue
- 1
- Pages
- 71-85
- ISSN
- 0301-0082
- Cited by
- 310
- References
- 3
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