ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Fibroblast growth factor (FGF)-2 and FGF receptor 3 are required for the development of the substantia nigra, and FGF-2 plays a crucial role for the rescue of dopaminergic neurons after 6-hydroxydopamine lesion.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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56 citing papers in PubMed, 120 citations in OpenAlex.
- Fibroblast Growth Factor-2 alone as an efficient inducer for differentiation of human bone marrow mesenchymal stem cells into dopaminergic neurons.Journal of biomedical science · 2014Trial
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- FGF-FGFR Signaling in Parkinson's Disease: Mechanistic Links to Ferroptosis and Neuroprotection.Brain sciences · 2026Review
- Peripheral and CSF protein quantification in Parkinson's disease and multiple system atrophy-the nucleic acid-linked immuno-sandwich assay.Brain communications · 2026Article
- Role of Fibroblast Growth Factors in Neurological Disorders: Insight into Therapeutic Approaches and Molecular Mechanisms.Molecular neurobiology · 2025Review
- Sex-Specific Differences in the Secretome of Oligodendrocyte Progenitor Cells Post Hyperoxic Stress.Journal of extracellular biology · 2025Article
- Photocuring CsA and bFGF-embedded hemostatic hydrogel promotes recovery from TBI by mitigating ferroptosis and neuroinflammation.iScience · 2025Article
- Molecular Determinants of A9 Dopaminergic Neurons.Neuromolecular medicine · 2025Review
- Extracellular Vesicles Derived from FGF2-Primed Astrocytes Against Mitochondrial and Synaptic Toxicities in Parkinson's Disease.International journal of nanomedicine · 2025Article
- Concomitant heparin use promotes skin graft donor site healing by basic fibroblast growth factor: A pilot prospective randomized controlled study.Contemporary clinical trials communications · 2024Article
- Unraveling the AKT/ERK cascade and its role in Parkinson disease.Archives of toxicology · 2024Review
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- Extracellular matrix protein anosmin-1 overexpression alters dopaminergic phenotype in the CNS and the PNS with no pathogenic consequences in a MPTP model of Parkinson's disease.Brain structure & function · 2023Article
- Chronic Voluntary Alcohol Consumption Alters Promoter Methylation and Expression ofInternational journal of molecular sciences · 2023Article
- Developmental pathways linked to the vulnerability of adult midbrain dopaminergic neurons to neurodegeneration.Frontiers in molecular neuroscience · 2022Review
- CSF MicroRNAs Reveal Impairment of Angiogenesis and Autophagy in Parkinson Disease.Neurology. Genetics · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basic fibroblast growth factor (FGF-2) is involved in the development and maintenance of the nervous system. Exogenous administration of FGF-2 increased dopaminergic (DA) graft survival in different animal models of Parkinson's disease. To study the physiological function of the endogenous FGF-2 system, we analyzed the nigrostriatal system of mice lacking FGF-2, mice overexpressing FGF-2, and FGF-receptor-3 (FGFR3)-deficient mice both after development and after 6-hydroxydopamine lesion. FGFR3-deficient mice (+/-) displayed a reduced number of DA neurons compared with the respective wild type. Whereas absence of FGF-2 led to significantly increased numbers of DA neurons, enhanced amount of the growth factor in mice overexpressing FGF-2 resulted in less tyrosine hydroxylase expression and a reduced DA cell density. The volumes of the substantia nigra were enlarged in both FGF-2(-/-) and in FGF-2 transgenic mice, suggesting an important role of FGF-2 for the establishment of the proper number of DA neurons and a normal sized substantia nigra during development. In a second set of experiments, the putative relevance of endogenous FGF-2 after neurotoxin application was investigated regarding the number of rescued DA neurons after partial 6-OHDA lesion. Interestingly, the results after lesion were directly opposed to the results after development: significantly less DA neurons survived in FGF-2(-/-) mice compared with wild-type mice. Together, the results indicate that FGFR3 is crucially involved in regulating the number of DA neurons. The lack of FGF-2 seems to be (over)compensated during development, but, after lesion, compensation mechanisms fail. The transgenic mice showed that endogenous FGF-2 protects DA neurons from 6-OHDA neurotoxicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.