ArticleToxicology letters2013
MPP+-induces PUMA- and p53-dependent, but ATF3-independent cell death.
Article in Toxicology letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Bbc3 Loss Enhances Survival and Protein Clearance in Neurons Exposed to the Organophosphate Pesticide Chlorpyrifos.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Activating transcription factor-4 promotes neuronal death induced by Parkinson's disease neurotoxins and α-synuclein aggregates.Cell death and differentiation · 2021Article
- Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins.Cell death and differentiation · 2021Review
- Article
- Mild closed head traumatic brain injury-induced changes in monoamine neurotransmitters in the trigeminal subnuclei of a rat model: mechanisms underlying orofacial allodynias and headache.Neural regeneration research · 2017Article
- Dopaminergic neuron-specific deletion of p53 gene is neuroprotective in an experimental Parkinson's disease model.Journal of neurochemistry · 2016Article
- Trigeminal neuroplasticity underlies allodynia in a preclinical model of mild closed head traumatic brain injury (cTBI).Neuropharmacology · 2016Article
- The E3 ubiquitin ligase seven in absentia homolog 1 may be a potential new therapeutic target for Parkinson's disease.Neural regeneration research · 2015Article
- Neurotoxin mechanisms and processes relevant to Parkinson's disease: an update.Neurotoxicity research · 2015Article
- Transcriptional and metabolic adaptation of human neurons to the mitochondrial toxicant MPP(+).Cell death & disease · 2014Article
- The Parkinsonian mimetic, 6-OHDA, impairs axonal transport in dopaminergic axons.Molecular neurodegeneration · 2014Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and depletion of striatal dopamine (DA), leading to a range of motor symptoms, including resting tremor, rigidity, bradykinesia and postural abnormalities. The neurotoxin (MPTP) and its active metabolite, 1-methyl-4-phenylpyridinium (MPP(+)), cause dopaminergic cell loss in a variety of animal species and produce symptoms similar to those seen in PD. Our lab has shown that MPP(+) activates cell stress pathways, including the unfolded protein response (UPR) in mouse primary mesencephalic cultures. The BH3-only protein, PUMA (p53 upregulated mediator of apoptosis), has been shown to be activated in response to many cellular stresses, including endoplasmic reticulum (ER) stress and UPR, and to induce cell death. Therefore, we hypothesized that PUMA may mediate MPP(+) toxicity. To test this hypothesis, we compared the response of primary mesencephalic cultures from wild-type and PUMA deficient (-/-) mice to MPP(+). We also utilized cultures from p53 -/- and activating transcription factor 3 (ATF3) -/- mice to further elucidate the pathways involved. These studies revealed that PUMA and p53, but not ATF3, are required for MPP(+)-induced cell death, suggesting that UPR activation is parallel to the induction of MPP(+)-induced cell death.
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