ArticleMolecular neurobiology2025
Microcystin-LR Exposure Damages Neurons by Inducing α-Syn Aggregation via MAPK4/GATA2/SNCA and PP2A/GRKs Pathways.
Article in Molecular neurobiology, 2025. 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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13 citing papers in PubMed.
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- The role of estrogen in Alzheimer's disease pathogenesis and therapeutic potential in women.Molecular and cellular biochemistry · 2025Review
- Brain-derived neurotrophic factor in older adults exposed to simulated indoor overheating.European journal of applied physiology · 2025Article
- Untargeted metabolomics unveils critical metabolic signatures in novel phenotypes of acute ischemic stroke.Metabolic brain disease · 2025Article
- The Role of Thrombo-inflammation in Ischemic Stroke: Focus on the Manipulation and Clinical Application.Molecular neurobiology · 2025Review
- Differential Expression of GABA Receptor-Related Genes in Alzheimer's Disease and the Positive Regulatory Role of Aerobic Exercise-From Genetic Screening to D-gal-induced AD-like Pathology Model.Neuromolecular medicine · 2024Article
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7 authors.
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Abstract
Microcystin-LR (MC-LR) is a natural neurotoxin with strong toxicity, and studies have demonstrated that chronic MC-LR exposure generated Parkinson-like dyskinesia in mice. Parkinson's disease (PD) is a neurologic degenerative disease mostly occurring in elderly people, and the progressive loss of dopaminergic neurons and the formation of Lewy bodies are the hallmark pathological features. The main component of Lewy bodies is α-synuclein (α-syn) encoded by the SNCA gene, and the copy number mutation of SNCA gene can promote the overexpression of α-syn. A mouse model of MC-LR exposure for 15 months was established to confirm the deposition of Lewy bodies. SH-SY5Y cells exposed to MC-LR were constructed as an in vitro model of PD, and the transcription factor that regulated the SNCA gene (the encoding gene of α-syn) was identified through the database. MC-LR enhanced the transcription level of SNCA gene and upregulated α-syn protein expression by promoting MAPK4 into the nucleus and binding to GATA2 295-480 fragment. In addition, MC-LR inhibited PP2A activity and activated GRKs kinase to promote α-syn phosphorylation at Ser129. These results suggest that MC-LR is involved in α-syn aggregate formation and PD pathogenesis by enhancing SNCA transcriptional activity to promote α-syn elevation via the MAPK4/GATA2 pathway and inducing α-syn phosphorylation via the PP2A/GRKs pathway.
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