ArticleAmerican journal of physiology. Cell physiology2005
Relative contribution of chloride channels and transporters to regulatory volume decrease in human glioma cells.
Article in American journal of physiology. Cell physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 110 citations in OpenAlex.
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- Construction of a solid Cox model for AML patients based on multiomics bioinformatic analysis.Frontiers in oncology · 2022Article
- Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021Review
- OSR1 phosphorylates the Smad2/3 linker region and induces TGF-β1 autocrine to promote EMT and metastasis in breast cancer.Oncogene · 2021Article
- Altered Spontaneous Glutamatergic and GABAergic Activity in the Peritumoral Cortex of Low-Grade Gliomas Presenting With History of Seizures.Frontiers in neuroscience · 2021Article
- Drug development in targeting ion channels for brain edema.Acta pharmacologica Sinica · 2020Article
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- ClC-5 Downregulation Induces Osteosarcoma Cell Apoptosis by Promoting Bax and tBid Complex Formation.Frontiers in oncology · 2020Article
- ClC5 Decreases the Sensitivity of Multiple Myeloma Cells to Bortezomib via Promoting Prosurvival Autophagy.Oncology research · 2018Article
- Combating malignant astrocytes: Strategies mitigating tumor invasion.Neuroscience research · 2018Review
- Scorpion and spider venoms in cancer treatment: state of the art, challenges, and perspectives.Journal of clinical and translational research · 2017Review
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- Effect of Crude Venom ofIranian journal of pharmaceutical research : IJPR · 2017Article
- Down-Regulation of ClC-3 Expression Reduces Epidermal Stem Cell Migration by Inhibiting Volume-Activated Chloride Currents.The Journal of membrane biology · 2016Article
- Seizures and gliomas--towards a single therapeutic approach.Nature reviews. Neurology · 2016Review
- Potential Roles of Amiloride-Sensitive Sodium Channels in Cancer Development.BioMed research international · 2016Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Primary brain tumors (gliomas) often present with peritumoral edema. Their ability to thrive in this osmotically altered environment prompted us to examine volume regulation in human glioma cells, specifically the relative contribution of Cl(-) channels and transporters to this process. After a hyposmotic challenge, cultured astrocytes, D54-MG glioma cells, and glioma cells from human patient biopsies exhibited a regulatory volume decrease (RVD). Although astrocytes were not able to completely reestablish their original prechallenge volumes, glioma cells exhibited complete volume recovery, sometimes recovering to a volume smaller than their original volumes (V(Post-RVD) < V(baseline)). In glioma cells, RVD was largely inhibited by treatment with a combination of Cl(-) channel inhibitors, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and Cd(2+) (V(Post-RVD) > 1.4*V(baseline)). Volume regulation was also attenuated to a lesser degree by the addition of R-(+)-[(2-n-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy]acetic acid (DIOA), a known K(+)-Cl(-) cotransporter (KCC) inhibitor. To dissect the relative contribution of channels vs. transporters in RVD, we took advantage of the comparatively high temperature dependence of transport processes vs. channel-mediated diffusion. Cooling D54-MG glioma cells to 15 degrees C resulted in a loss of DIOA-sensitive volume regulation. Moreover, at 15 degrees C, the channel blockers NPPB + Cd(2+) completely inhibited RVD and cells behaved like perfect osmometers. The calculated osmolyte flux during RVD under these experimental conditions suggests that the relative contribution of Cl(-) channels vs. transporters to this process is approximately 60-70% and approximately 30-40%, respectively. Finally, we identified several candidate proteins that may be involved in RVD, including the Cl(-) channels ClC-2, ClC-3, ClC-5, ClC-6, and ClC-7 and the transporters KCC1 and KCC3a.
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