ArticleMolecular neurobiology2014
The proform of glia cell line-derived neurotrophic factor: a potentially biologically active protein.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Inhibition of tRF- 02514 in Extracellular Vesicles Preserves Microglia Pyroptosis and Protects Against Parkinson's Disease.Molecular neurobiology · 2025Article
- Procalcitonin contributes to hippocampal neuronal damage and impairment of LTP: implications for cognitive dysfunction in LPS-induced neuroinflammation rat model.Archives of microbiology · 2025Article
- Molecular signatures of astrocytes and microglia maladaptive responses to acute stress are rescued by a single administration of ketamine in a rodent model of PTSD.Translational psychiatry · 2024Article
- Cellular Localization and Distribution of TGF-β1, GDNF and PDGF-BB in the Adult Primate Central Nervous System.Neurochemical research · 2023Article
- High-Frequency Repetitive Transcranial Magnetic Stimulation Regulates Astrocyte Activation by Modulating the Endocannabinoid System in Parkinson's Disease.Molecular neurobiology · 2022Article
- Article
- Looking for a Treatment for the Early Stage of Alzheimer's Disease: Preclinical Evidence with Co-Ultramicronized Palmitoylethanolamide and Luteolin.International journal of molecular sciences · 2020Article
- Sensorimotor gating deficits in "two-hit" models of schizophrenia risk factors.Schizophrenia research · 2018Review
- Neuroprotective effects of the gliopeptide ODN in an in vivo model of Parkinson's disease.Cellular and molecular life sciences : CMLS · 2018Article
- Behavioral sequelae of astrocyte dysfunction: focus on animal models of schizophrenia.Schizophrenia research · 2016Review
- Effects of Hindlimb Unweighting on MBP and GDNF Expression and Morphology in Rat Dorsal Root Ganglia Neurons.Neurochemical research · 2016Article
- Gas1 up-regulation is inducible and contributes to cell apoptosis in reactive astrocytes in the substantia nigra of LPS and MPTP models.Journal of neuroinflammation · 2016Article
- Effects of striatal transplantation of cells transfected with GDNF gene without pre- and pro-regions in mouse model of Parkinson's disease.BMC neuroscience · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidences have revealed that the proforms of several neurotrophins including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT3), by binding to p75 neurotrophin receptor and sortilin, could induce neuronal apoptosis and are implicated in the pathogenesis of various neurodegenerative diseases. The glial cell line-derived neurotrophic factor (GDNF), one of the most potent useful neurotrophic factors for the treatment of Parkinson's disease (PD), is firstly synthesized as the proform (proGDNF) like other neurotrophin NGF, BDNF, and NT3. However, little is known about proGDNF expression and secretion under physiological as well as pathological states in vivo or in vitro. In this study, we investigated the expression profile and dynamic changes of proGDNF in brains of aging and PD animal models, with the interesting finding that proGDNF was a predominant form of GDNF with molecular weight of about 36 kDa by reducing and nonreducing immunoblots in adult brains and was unregulated in the aging, lipopolysaccharide (LPS), and 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP) insult. We further provided direct evidence that accompanied activation of primary astrocytes as well as C6 cell line induced by LPS stimulation, proGDNF was increasingly synthesized and released as the uncleaved form in cell culture. Taken together, our results strongly suggest that proGDNF may be a biologically active protein and has specific effects on the cells close to its secreting site, and a potentially important role of proGDNF signaling in the brains, in the glia-neuronal interaction or in the pathogenesis of PD, should merit further investigation.
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