ArticleProteome science2014
The rat striatum responds to nigro-striatal degeneration via the increased expression of proteins associated with growth and regeneration of neuronal circuitry.
Article in Proteome science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
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- Intranasal delivery of dodecyl creatine ester alleviates motor deficits and increases dopamine levels in a 6-OHDA rat model of parkinsonism.Frontiers in aging neuroscience · 2025Article
- AAV9-mediated SMN gene therapy rescues cardiac desmin but not lamin A/C and elastin dysregulation in Smn2B/- spinal muscular atrophy mice.Human molecular genetics · 2023Article
- The mitochondrial protein Sideroflexin 3 (SFXN3) influences neurodegeneration pathways in vivo.The FEBS journal · 2022Article
- Analysis of the Neuroproteome Associated With Cell Therapy After Intranigral Grafting in a Mouse Model of Parkinson Disease.Frontiers in neuroscience · 2021Article
- Lamin A/C dysregulation contributes to cardiac pathology in a mouse model of severe spinal muscular atrophy.Human molecular genetics · 2019Article
- Altered mitochondrial bioenergetics are responsible for the delay in Wallerian degeneration observed in neonatal mice.Neurobiology of disease · 2019Article
- Characterization of Xenopus laevis guanine deaminase reveals new insights for its expression and function in the embryonic kidney.Developmental dynamics : an official publication of the American Association of Anatomists · 2019Article
- Article
- A Novel Short Isoform of Cytosolic PSD-95 Interactor (Cypin) Regulates Neuronal Development.Molecular neurobiology · 2018Article
- Morphological Changes in a Severe Model of Parkinson's Disease and Its Suitability to Test the Therapeutic Effects of Microencapsulated Neurotrophic Factors.Molecular neurobiology · 2017Article
- Sideroflexin 3 is an α-synuclein-dependent mitochondrial protein that regulates synaptic morphology.Journal of cell science · 2017Article
- Mechanisms and Consequences of Dopamine Depletion-Induced Attenuation of the Spinophilin/Neurofilament Medium Interaction.Neural plasticity · 2017Article
- Proteomic Profiling of Cranial (Superior) Cervical Ganglia Reveals Beta-Amyloid and Ubiquitin Proteasome System Perturbations in an Equine Multiple System Neuropathy.Molecular & cellular proteomics : MCP · 2015Article
- Topographical Distribution of Morphological Changes in a Partial Model of Parkinson's Disease--Effects of Nanoencapsulated Neurotrophic Factors Administration.Molecular neurobiology · 2015Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundIdiopathic Parkinson's disease is marked by degeneration of dopamine neurons projecting from the substantia nigra to the striatum. Although proteins expressed by the target striatum can positively affect the viability and growth of dopaminergic neurons, very little is known about the molecular response of the striatum as nigro-striatal denervation progresses. Here, iTRAQ labelling and MALDI TOF/TOF mass spectrometry have been used to quantitatively compare the striatal proteome of rats before, during, and after 6-OHDA induced dopamine denervation.
resultsiTRAQ analysis revealed the differential expression of 50 proteins at 3 days, 26 proteins at 7 days, and 34 proteins at 14 days post-lesioning, compared to the unlesioned striatum. While the denervated striatum showed a reduced expression of proteins associated with the loss of dopaminergic input (e.g., TH and DARPP-32), there was an increased expression of proteins associated with regeneration and growth of neurites (e.g., GFAP). In particular, the expression of guanine deaminase (GDA, cypin) - a protein known to be involved in dendritic branching - was significantly increased in the striatum at 3, 7 and 14 days post-lesioning (a finding verified by immunohistochemistry).
conclusionsTogether, these findings provide evidence to suggest that the response of the normal mammalian striatum to nigro-striatal denervation includes the increased expression of proteins that may have the capacity to facilitate repair and growth of neuronal circuitry.
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