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Updated: May 11, 2026
Imaging Intracellular Ca2+ Signals in Striatal Astrocytes from Adult Mice Using Genetically-encoded Calcium Indicators
Published on: November 19, 2014
NFATc3 promotes Ca(2+) -dependent MMP3 expression in astroglial cells
Fernando Neria1, María del Carmen Serrano-Perez, Patricia Velasco
1Unidad de Neuroinflamación, Área de Biología Celular y del Desarrollo, Unidad Funcional de Investigación en Enfermedades Crónicas, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.
Increased intracellular calcium ([Ca(2+) ]i) activates the calcineurin (CN)/nuclear factor of activated T cells (NFAT) pathway, driving matrix metalloproteinase 3 (Mmp3) expression in astrocytes, crucial for neuroinflammation after brain injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Intracellular calcium ([Ca(2+) ]i) increase is a key mediator of astrocyte signaling.
- The calcineurin (CN)/nuclear factor of activated T cells (NFAT) pathway is central to inflammatory events.
Purpose of the Study:
- To analyze matrix metalloproteinase 3 (Mmp3) expression in response to increased [Ca(2+) ]i.
- To investigate the role of the CN/NFAT pathway in regulating Mmp3 expression in astrocytes.
Main Methods:
- Overexpression of active NFATc3 in astrocytes.
- Stimulation with calcium ionophore (Io) and Bz-ATP.
- Inhibition studies using cyclosporin A (CsA) and actinomycin D.
- Luciferase reporter assay for Mmp3 promoter activity.
- In vivo stab-wound brain injury model.
Main Results:
- NFATc3 overexpression and [Ca(2+) ]i increase induced astrocyte Mmp3 expression.
- CN/NFAT pathway inhibition blocked Mmp3 upregulation.
- Mmp3 regulation occurred at the transcriptional level.
- MMP3 expression was observed in astrocytes in a brain injury model.
Conclusions:
- Astrocyte Mmp3 expression is regulated by the Ca(2+) /CN/NFAT pathway.
- This pathway plays a role in the early neuroinflammatory response to brain injury.
- Targeting this pathway may offer therapeutic strategies for brain injury recovery.
