ArticleAmerican journal of physiology. Cell physiology2009
Metabolic inhibition increases activity of connexin-32 hemichannels permeable to Ca2+ in transfected HeLa cells.
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 75 citations in OpenAlex.
- A fully human IgG1 antibody targeting connexin 32 extracellular domain blocks CMTX1 hemichannel dysfunction in an in vitro model.Cell communication and signaling : CCS · 2024Article
- A pore locus in the E1 domain differentially regulates Cx26 and Cx30 hemichannel function.The Journal of general physiology · 2024Article
- Calcium Regulation of Connexin Hemichannels.International journal of molecular sciences · 2024Review
- Connexin channels and hemichannels are modulated differently by charge reversal at residues forming the intracellular pocket.Biological research · 2024Article
- Article
- Measurement of CaMethods in molecular biology (Clifton, N.J.) · 2024Article
- Purification, Reconstitution, and Functional Analysis of Connexin Hemichannels.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Hemichannels contribute to mitochondrial CaFrontiers in cell and developmental biology · 2024Article
- Inhibition of connexin hemichannels alleviates neuroinflammation and hyperexcitability in temporal lobe epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A Quantitative Assay for CaInternational journal of molecular sciences · 2022Article
- Extracellular Cysteines Are Critical to Form Functional Cx46 Hemichannels.International journal of molecular sciences · 2022Article
- Article
- Circulating levels of ATP is a biomarker of HIV cognitive impairment.EBioMedicine · 2020Article
- The Neuroglial Dialog Between Cannabinoids and Hemichannels.Frontiers in molecular neuroscience · 2018Article
- Physiology of Astroglia.Physiological reviews · 2018Review
- Contribution of Astroglial Cx43 Hemichannels to the Modulation of Glutamatergic Currents by D-Serine in the Mouse Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- On Biophysical Properties and Sensitivity to Gap Junction Blockers of Connexin 39 Hemichannels Expressed in HeLa Cells.Frontiers in physiology · 2017Article
- Linoleic acid permeabilizes gastric epithelial cells by increasing connexin 43 levels in the cell membrane via a GPR40- and Akt-dependent mechanism.Biochimica et biophysica acta · 2016Article
- Connexin and pannexin signaling pathways, an architectural blueprint for CNS physiology and pathology?Cellular and molecular life sciences : CMLS · 2015Review
- Role of Akt and Ca2+ on cell permeabilization via connexin43 hemichannels induced by metabolic inhibition.Biochimica et biophysica acta · 2015Article
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4 authors at 2 institutions in 2 countries.
Funding
Abstract
Numerous cell types express functional connexin (Cx) hemichannels (HCs), and membrane depolarization and/or exposure to a divalent cation-free bathing solution (DCFS) have been shown to promote HC opening. However, little is known about conditions that can promote HC opening in the absence of strong depolarization and when extracellular divalent cation concentrations remain at physiological levels. Here the effects of metabolic inhibition (MI), an in vitro model of ischemia, on the activity of mouse Cx32 HCs were examined. In HeLa cells stably transfected with mouse Cx32 (HeLa-Cx32), MI induced an increase in cellular permeability to ethidium (Etd). The increase in Etd uptake was directly related to an increase in levels of Cx32 HCs present at the cell surface. Moreover, MI increased membrane currents in HeLa-Cx32 cells. Underlying these currents were channels exhibiting a unitary conductance of approximately 90 pS, consistent with Cx32 HCs. These currents and Etd uptake were blocked by HC inhibitors. The increase in Cx32 HC activity was preceded by a rapid reduction in mitochondrial membrane potential and a rise in free intracellular Ca(2+) concentration ([Ca(2+)](i)). The increase in free [Ca(2+)](i) was prevented by HC blockade or exposure to extracellular DCFS and was virtually absent in parental HeLa cells. Moreover, inhibition of Cx32 HCs expressed by HeLa cells in low-confluence cultures drastically reduced cell death induced by oxygen-glucose deprivation, which is a more physiological model of ischemia-reperfusion. Thus HC blockade could reduce the increase in free [Ca(2+)](i) and cell death induced by ischemia-like conditions in cells expressing Cx32 HCs.
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