Biomolecular and Functional Changes in a Culture of Microglial Cells Caused by Long-Term Exposure to AlCl3
A V Sentyabreva1,2, M A Diatroptova3, E A Miroshnichenko3,4
1Avtsyn Research Institute of Human Morphology, Petrovsky National Research Centre of Surgery, Moscow, Russia. alexandraasentyabreva@gmail.com.
Abstract:
Inflammaging is one of the main risk factors for the development and progression of age-related diseases. The increase in the proinflammatory background and ROS production can lead to persistent activation and dysfunction of microglial cells. The biomolecular and functional changes in microglial cells after long-term exposure to prooxidant aluminum chloride were studied in in vitro experiment. BV2 cells were cultured in the presence of 0.5 and 1 mM AlCl3 for 70 or 140 h. The intensity of ROS production, apoptosis, and M1/M2 phenotype polarization of microglia were assessed by flow cytometry, qPCR-RT, and ELISA. Cells cultured with 0.5 mM AlCl3 showed signs of "healthy aging", while the higher concentration (1 mM) of AlCl3 led to persistent activation of microglia. The data obtained can be used for in vitro modeling of inflammaging and related physiological and pathological processes.
Insights
Aluminum chloride (AlCl3) exposure in microglia cells can model inflammaging. Lower AlCl3 concentrations suggest healthy aging, while higher concentrations induce persistent microglial activation, crucial for age-related disease research.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Inflammaging, a chronic proinflammatory state, drives age-related diseases.
- Microglial cells, key immune cells in the brain, become activated and dysfunctional due to increased reactive oxygen species (ROS) and inflammation.
- Aluminum chloride (AlCl3) is a prooxidant that may influence microglial aging.
Purpose of the Study:
- To investigate the biomolecular and functional effects of long-term aluminum chloride exposure on microglial cells.
- To model inflammaging and associated cellular changes in vitro.
- To determine the dose-dependent effects of AlCl3 on microglial activation and phenotype.
Main Methods:
- BV2 microglial cell line cultured with 0.5 mM and 1 mM AlCl3 for 70 or 140 hours.
- Assessment of reactive oxygen species (ROS) production via flow cytometry.
- Evaluation of apoptosis and M1/M2 phenotype polarization using qPCR-RT and ELISA.
Main Results:
- Low-dose AlCl3 (0.5 mM) exposure resulted in characteristics of "healthy aging" in microglia.
- High-dose AlCl3 (1 mM) induced persistent activation and dysfunction of microglial cells.
- AlCl3 exposure modulated ROS production, apoptosis, and M1/M2 polarization.
Conclusions:
- Aluminum chloride can be used to create an in vitro model of inflammaging.
- Microglial responses to AlCl3 are concentration-dependent, mimicking aspects of aging.
- This model aids in studying age-related diseases linked to microglial dysfunction.
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