ArticleMolecular neurobiology2013
Involvement of volume-activated chloride channels in H2O 2 preconditioning against oxidant-induced injury through modulating cell volume regulation mechanisms and membrane permeability in PC12 cells.
Article in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 17 citations in OpenAlex.
- SGK1 mediates the hypotonic protective effect against HActa pharmacologica Sinica · 2020Article
- Mitochondrial Complex I Is an Essential Player in LPS-Induced Preconditioning in Differentiated PC12 Cells.Iranian journal of pharmaceutical research : IJPR · 2019Article
- SOPflugers Archiv : European journal of physiology · 2017Article
- Trypanosome Lytic Factor-1 Initiates Oxidation-stimulated Osmotic Lysis of Trypanosoma brucei brucei.The Journal of biological chemistry · 2016Article
- The rs3737964 single-nucleotide polymorphism of the chloride channel-6 gene as a risk factor for coronary heart disease.Molecular genetics & genomic medicine · 2015Article
- Volume-sensitive chloride channels are involved in cisplatin treatment of osteosarcoma.Molecular medicine reports · 2015Article
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11 authors at 4 institutions in 1 country.
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Abstract
The functions of chloride channels in preconditioning-induced cell protection remain unclear. In this report, we show that the volume-activated chloride channels play a key role in hydrogen peroxide (H2O2) preconditioning-induced cell protection in pheochromocytoma PC12 cells. The preconditioning with 100 μM H2O2 for 90 min protected the cells from injury induced by long period exposure to 300 μM H2O2. The protective effect was attenuated by pretreatment with the chloride channel blockers, 5-nitro-2-3-phenylpropylamino benzoic acid (NPPB) and tamoxifen. H2O2 preconditioning directly activated a chloride current, which was moderately outward-rectified and sensitive to the chloride channel blockers and hypertonicity-induced cell shrinkage. H2O2 preconditioning functionally up-regulated the activities of volume-activated chloride channels and enhanced the regulatory volume decrease when exposure to extracellular hypotonic challenges. In addition, acute application of H2O2 showed distinctive actions on cell volume and membrane permeability in H2O2 preconditioned cells. In H2O2 preconditioned cells, acute application of 300 μM H2O2 first promptly induced a decrease of cell volume and enhancement of cell membrane permeability, and then, cell volume was maintained at a relatively stable level and the facilitation of membrane permeability was reduced. Conversely, in control cells, 300 μM H2O2 induced a slow but persistent apoptotic volume decrease (AVD) and facilitation of membrane permeability. H2O2 preconditioning also significantly up-regulated the expression of ClC-3 protein, the molecular candidate of the volume-activated chloride channel. These results suggest that H2O2 preconditioning can enhance the expression and functional activities of volume-activated chloride channels, thereby modulate cell volume and cell membrane permeability, which may contribute to neuroprotection against oxidant-induced injury.
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