ArticleInternational journal of molecular sciences2022
Alterations in UPR Signaling by Methylmercury Trigger Neuronal Cell Death in the Mouse Brain.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 12 citations in OpenAlex.
- Protective effects of dietary Cucurbita pepo on oxidative damage, histopathological alterations, and endoplasmic reticulum stress in the brain and gills of Oreochromis niloticus exposed to trace elements.Veterinary research communications · 2025Article
- Endoplasmic reticulum: the target of chlamydial manipulation.Archives of microbiology · 2025Review
- Environmental adversity, endoplasmic reticulum stress, and neurogenesis.Neurotoxicology · 2025Review
- Therapeutic potential of 4-phenylbutyric acid against methylmercury-induced neuronal cell death in mice.Archives of toxicology · 2025Article
- Treadmill exercise protects against methylmercury neurotoxicity by increasing BDNF in the mouse brain.Environmental health and preventive medicine · 2025Article
- Mechanisms Underlying Sensory Nerve-Predominant Damage by Methylmercury in the Peripheral Nervous System.International journal of molecular sciences · 2024Article
- Methylmercury exposure at dosage conditions that do not affect growth can impair memory in adolescent mice.Toxicological research · 2024Article
- Characterization of pathological changes in the olfactory system of mice exposed to methylmercury.Archives of toxicology · 2024Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylmercury (MeHg), an environmental toxicant, induces neuronal cell death and injures specific areas of the brain. MeHg is known to induce oxidative and endoplasmic reticulum (ER) stress. The unfolded protein response (UPR) pathway has a dual nature in that it regulates and protects cells from an overload of improperly folded proteins in the ER, whereas excessively stressed cells are eliminated by apoptosis. Oxidative stress/ER stress induced by methylmercury exposure may tilt the UPR toward apoptosis, but there is little in vivo evidence of a direct link to actual neuronal cell death. Here, by using the ER stress-activated indicator (ERAI) system, we investigated the time course signaling alterations of UPR in vivo in the most affected areas, the somatosensory cortex and striatum. In the ERAI-Venus transgenic mice exposed to MeHg (30 or 50 ppm in drinking water), the ERAI signal, which indicates the activation of the cytoprotective pathway of the UPR, was only transiently enhanced, whereas the apoptotic pathway of the UPR was persistently enhanced. Furthermore, detailed analysis following the time course showed that MeHg-induced apoptosis is strongly associated with alterations in UPR signaling. Our results suggest that UPR modulation could be a therapeutic target for treating neuropathy.
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