Polyamines preserve connexin 43-mediated gap junctional communication during intracellular hypercalcemia and acidosis

Changes in the regulation, formation, and gating of connexin-based gap junction channels occur in various disorders. It has been shown that H and Ca are involved in the regulation of gap junctional communication. Ischemia-induced intracellular acidification and Ca overload lead to closure of gap jun...

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Published in:Neuroreport Vol. 28; no. 4; pp. 208 - 213
Main Authors: Kucheryavykh, Lilia Y, Benedikt, Jan, Cubano, Luis A, Skatchkov, Serguei N, Bukauskas, Feliksas F, Kucheryavykh, Yuriy V
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Language:English
Published: England 01-03-2017
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Abstract Changes in the regulation, formation, and gating of connexin-based gap junction channels occur in various disorders. It has been shown that H and Ca are involved in the regulation of gap junctional communication. Ischemia-induced intracellular acidification and Ca overload lead to closure of gap junctions and inhibit an exchange by ions and small molecules throughout the network of cells in the heart, brain, and other tissues. In this study, we examined the role of the polyamines in the regulation of connexin 43 (Cx43)-based gap junction channels under elevated intracellular concentrations of hydrogen ([H]i) and calcium ([Ca]i) ions. Experiments, conducted in Novikoff and A172 human glioblastoma cells, which endogenously express Cx43, showed that polyamines prevent downregulation of Cx43-mediated gap junctional communication caused by elevated [Ca]i and [H]i, accompanying ischemic and other pathological conditions. siRNA knockdown of Cx43 significantly reduces gap junctional communication, indicating that Cx43 gap junctions are the targets for spermine regulation.
AbstractList Changes in the regulation, formation, and gating of connexin-based gap junction channels occur in various disorders. It has been shown that H and Ca are involved in the regulation of gap junctional communication. Ischemia-induced intracellular acidification and Ca overload lead to closure of gap junctions and inhibit an exchange by ions and small molecules throughout the network of cells in the heart, brain, and other tissues. In this study, we examined the role of the polyamines in the regulation of connexin 43 (Cx43)-based gap junction channels under elevated intracellular concentrations of hydrogen ([H]i) and calcium ([Ca]i) ions. Experiments, conducted in Novikoff and A172 human glioblastoma cells, which endogenously express Cx43, showed that polyamines prevent downregulation of Cx43-mediated gap junctional communication caused by elevated [Ca]i and [H]i, accompanying ischemic and other pathological conditions. siRNA knockdown of Cx43 significantly reduces gap junctional communication, indicating that Cx43 gap junctions are the targets for spermine regulation.
Author Benedikt, Jan
Kucheryavykh, Lilia Y
Cubano, Luis A
Kucheryavykh, Yuriy V
Skatchkov, Serguei N
Bukauskas, Feliksas F
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  organization: Departments of aBiochemistry bPhysiology cAnatomy and Cell Biology, School of Medicine, Universidad Central del Caribe, Bayamón, Puerto Rico dDominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, New York, New York, USA eInstitute of Cardiology, Lithuanian University of Health Sciences, Kaunas, Lithuania
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Snippet Changes in the regulation, formation, and gating of connexin-based gap junction channels occur in various disorders. It has been shown that H and Ca are...
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SubjectTerms Acidosis
Animals
Calcium
Cell Line, Tumor
Connexin 43 - metabolism
Gap Junctions - drug effects
Gap Junctions - physiology
Humans
Hydrogen-Ion Concentration
Hypercalcemia
Neurons - metabolism
Neurons - physiology
Polyamines - administration & dosage
Rats
Spermine - administration & dosage
Title Polyamines preserve connexin 43-mediated gap junctional communication during intracellular hypercalcemia and acidosis
URI https://www.ncbi.nlm.nih.gov/pubmed/28134630
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