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Calcium Dyshomeostasis Alters CCL5 Signaling in Differentiated PC12 Cells
Tomasz Radzik1, Tomasz Boczek1,2, Bozena Ferenc1
1Department of Molecular Neurochemistry, Medical University, 6/8 Mazowiecka Str., 92-215 Lodz, Poland.
Biomed Research International
|April 30, 2019
Summary
Reduced plasma membrane Ca2+-ATPase (PMCA) function impairs calcium clearance in neurons. This, combined with inflammatory chemokine CCL5, exacerbates calcium dyshomeostasis, potentially leading to neurodegeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Plasma membrane Ca2+-ATPase (PMCA) regulates cellular calcium, with neuron-specific isoforms PMCA2 and PMCA3 crucial for calcium homeostasis.
- Aging impairs brain PMCA function, potentially contributing to neurodegenerative diseases via disrupted calcium signaling.
- Proinflammatory chemokine CCL5 exacerbates calcium release from the endoplasmic reticulum.
Purpose of the Study:
- To investigate the impact of reduced PMCA2 or PMCA3 expression on neuronal calcium transients in response to CCL5.
- To analyze the expression of chemokine receptors and IP3 receptors under conditions of PMCA deficiency.
Main Methods:
- Utilized stably transfected PC12 cells with downregulated PMCA2 or PMCA3 to mimic aged neurons.
- Assessed calcium transients using Fluo-4 reagent after CCL5 stimulation.
- Evaluated chemokine receptor and IP3 receptor expression via Western blot and qRT-PCR.
Main Results:
- Cells with reduced PMCA expression showed increased Ca2+ release mediated by IP3-sensitive receptors upon CCL5 stimulation.
- Calcium clearance was significantly prolonged in PMCA-deficient cells.
- Altered expression of CCR5 and IP3 receptors was observed in PMCA-reduced cell lines.
Conclusions:
- PMCA2 deficiency is more detrimental to neuronal cells than PMCA3 deficiency regarding calcium overload.
- Inflammatory CCL5 action and impaired calcium homeostasis due to PMCA reduction can lead to progressive neuronal degeneration and death.
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