Proinflammatory Cytokines and Potassium Channels in the Kidney
Proinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K+) channels induces changes in transepithel...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/362768 |
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| author | Kazuyoshi Nakamura Hikaru Hayashi Manabu Kubokawa |
| author_facet | Kazuyoshi Nakamura Hikaru Hayashi Manabu Kubokawa |
| author_sort | Kazuyoshi Nakamura |
| collection | DOAJ |
| description | Proinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K+) channels induces changes in transepithelial transport of solutes and water in the kidney, since K+ channels in tubule cells are indispensable for formation of membrane potential which serves as a driving force for the transepithelial transport. Altered K+ channel activity may be involved in renal cell dysfunction during inflammation. Although little information was available regarding the effects of proinflammatory cytokines on renal K+ channels, reports have emerged during the last decade. In human proximal tubule cells, interferon-γ showed a time-dependent biphasic effect on a 40 pS K+ channel, that is, delayed suppression and acute stimulation, and interleukin-1β acutely suppressed the channel activity. Transforming growth factor-β1 activated KCa3.1 K+ channel in immortalized human proximal tubule cells, which would be involved in the pathogenesis of renal fibrosis. This review discusses the effects of proinflammatory cytokines on renal K+ channels and the causal relationship between the cytokine-induced changes in K+ channel activity and renal dysfunction. |
| format | Article |
| id | doaj-art-e860c79a400744ce8debd446dfccf7f4 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-e860c79a400744ce8debd446dfccf7f42025-02-03T06:13:11ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/362768362768Proinflammatory Cytokines and Potassium Channels in the KidneyKazuyoshi Nakamura0Hikaru Hayashi1Manabu Kubokawa2Department of Physiology, Iwate Medical University School of Medicine, 2-1-1 Nishitokuta, Yahaba, Iwate 028-3694, JapanDepartment of Physiology, Iwate Medical University School of Medicine, 2-1-1 Nishitokuta, Yahaba, Iwate 028-3694, JapanDepartment of Physiology, Iwate Medical University School of Medicine, 2-1-1 Nishitokuta, Yahaba, Iwate 028-3694, JapanProinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K+) channels induces changes in transepithelial transport of solutes and water in the kidney, since K+ channels in tubule cells are indispensable for formation of membrane potential which serves as a driving force for the transepithelial transport. Altered K+ channel activity may be involved in renal cell dysfunction during inflammation. Although little information was available regarding the effects of proinflammatory cytokines on renal K+ channels, reports have emerged during the last decade. In human proximal tubule cells, interferon-γ showed a time-dependent biphasic effect on a 40 pS K+ channel, that is, delayed suppression and acute stimulation, and interleukin-1β acutely suppressed the channel activity. Transforming growth factor-β1 activated KCa3.1 K+ channel in immortalized human proximal tubule cells, which would be involved in the pathogenesis of renal fibrosis. This review discusses the effects of proinflammatory cytokines on renal K+ channels and the causal relationship between the cytokine-induced changes in K+ channel activity and renal dysfunction.http://dx.doi.org/10.1155/2015/362768 |
| spellingShingle | Kazuyoshi Nakamura Hikaru Hayashi Manabu Kubokawa Proinflammatory Cytokines and Potassium Channels in the Kidney Mediators of Inflammation |
| title | Proinflammatory Cytokines and Potassium Channels in the Kidney |
| title_full | Proinflammatory Cytokines and Potassium Channels in the Kidney |
| title_fullStr | Proinflammatory Cytokines and Potassium Channels in the Kidney |
| title_full_unstemmed | Proinflammatory Cytokines and Potassium Channels in the Kidney |
| title_short | Proinflammatory Cytokines and Potassium Channels in the Kidney |
| title_sort | proinflammatory cytokines and potassium channels in the kidney |
| url | http://dx.doi.org/10.1155/2015/362768 |
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