Astrocyte Culture medium

Cosmo Bio

Catalog No.: PMC-ASTM

Product Description

Culture medium for astrocytes (Cat. No. PMC-AST01C-COS and PMC-AST02C-COS).

Heterogeneous Roles of Glial Cells: Neurotoxicity or Neuroprotection

Astrocytes are the most abundant glial cells in the brain. Their primary roles include maintaining neuronal structure, regulating homeostasis, and supporting the integrity of the blood–brain barrier. However, conditions such as inflammation, liver injury, and neurodegeneration can induce morphological changes in astrocytes—such as the formation of Alzheimer’s type II astrocytes and fibrous astrocytes—ultimately leading to gliosis.

Moreover, stimulation by cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and interferon (IFN)-γ has been shown to exert neurotoxic effects, including the production of arachidonic acid metabolites, reactive oxygen species (ROS), and nitric oxide (NO). Conversely, astrocytes also exhibit neuroprotective functions in disorders such as Parkinson’s disease, including antioxidant activity through the secretion of glutathione (GSH) and modulation of synaptic transmission via the release of neurotransmitters such as glutamate, ATP, and D-serine.

Microglia, on the other hand, are primarily responsible for removing degenerated cells through antigen presentation and macrophage-like phagocytosis during inflammation. However, microglia expressing TNF-α, IL-1β, and IFN-γ have been identified in regions affected by neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Although activated microglia can exhibit neurotoxic effects through the production of ROS and NO, they also collaborate with astrocytes to secrete neuroprotective factors such as nerve growth factor (NGF), neurotrophins, and IL-6, thereby promoting neurogenesis from neural stem and progenitor cells.

In summary, astrocytes and microglia display heterogeneous and context-dependent functions. The complex and dynamic roles of glial cells in different physiological and pathological environments remain incompletely understood, and further research is needed to elucidate these mechanisms.

References

1. Blasko, I., Sta mpfer-Kountchev, M., Ro batscher, P., Veerhuis, R., Eikelenboom, P., & Grubeck-Loebenstein, B. (2004). Aging cell , 3(4), 169-76.
2. Maragakis, NJ, & Rothstein, JD (2006). Nature clinical practice Neurology , 2(12), 679-89.
3. Sawada, M. (2009). Parkinsonism & related disorders , 15 Suppl 1, S39 41.
4. Johansson, C., Momma, S., & Clarke, D. (1999). Cell , 96, 25-34.