Contributing to Understand the Crosstalk between Brain and Periphery in Methylmercury Intoxication: Neurotoxicity and Extracellular Vesicles.
Gabriela de Paula ArrifanoMarcus Augusto-OliveiraMegan Sealey-BrightJaezah ZainalLuciana ImbiribaLuanna Melo Pereira FernandesCristiane Socorro Ferraz MaiaDaniel Clive AnthonyMaria Elena Crespo-LópezPublished in: International journal of molecular sciences (2021)
Human exposure to methylmercury (MeHg) is currently high in regions such as the Amazon. Understanding the molecular changes associated with MeHg-induced neurotoxicity and the crosstalk with the periphery is essential to support early diagnoses. This work aimed to evaluate cellular and molecular changes associated with behavioral alterations in MeHg acute exposure and the possible changes in extracellular vesicles (EVs) number and S100β content. Adults male Wistar rats were orally treated with 5 mg/kg for four days. Behavioral performance, molecular and histological changes in the cerebellum, and plasma EVs were assessed. MeHg-intoxicated animals performed significantly worse in behavioral tests. MeHg increased the number of GFAP+ cells and GFAP and S100β mRNA expression in the cerebellum but no change in NeuN+ or IBA-1+ cells number was detected. The number of exosomes isolated from plasma were decreased by the metal. S100B mRNA was detected in circulating plasma EVs cargo in MeHg exposure. Though preliminary, our results suggest astrocytic reactivity is displaying a protective role once there was no neuronal death. Interestingly, the reduction in exosomes number could be a new mechanism associated with MeHg-induced neurotoxicity and plasma EVs could represent a source of future biomarkers in MeHg intoxication.
Keyphrases
- induced apoptosis
- high glucose
- cell cycle arrest
- stem cells
- mesenchymal stem cells
- endothelial cells
- drug induced
- diabetic rats
- single molecule
- oxidative stress
- liver failure
- endoplasmic reticulum stress
- multiple sclerosis
- brain injury
- white matter
- cell death
- cell proliferation
- respiratory failure
- binding protein
- hepatitis b virus
- cerebral ischemia
- stress induced
- extracorporeal membrane oxygenation
- induced pluripotent stem cells