Interleukin-1β suppresses activity of an inwardly rectifying K+ channel in human renal proximal tubule cells

Nakamura, Kazuyoshi; You, Ke; Kubokawa, Masaru

doi:10.1007/s12576-013-0275-6

Cited by 3 publications

(8 citation statements)

References 42 publications

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“…The basolateral K + channels provide the driving force for the apical Na + entry by forming the cell-negative potential and serving as the K + recycling pathway coupled with the Na + -K + -ATPase activity [ 1 , 2 ]. The effects of cytokines on the K + channels in human proximal tubule cells have recently been reported, using the patch-clamp technique [ 36 – 38 ]. In cultured human proximal tubule cells (RPTECs) derived from the normal kidney, an inwardly rectifying K + channel with an inward conductance of 40 pS is predominantly observed under the control condition [ 39 ].…”

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

“…The 40 pS K + channel possesses a relatively high open probability (0.8 on average) with no voltage dependence [ 39 ] and contributes to the formation of cell-negative potential [ 40 ]. Furthermore, the activity of this K + channel is regulated by intracellular ATP [ 39 ], pH [ 39 ], and protein phosphorylation processes mediated by protein kinase A (PKA) [ 39 ] and protein kinase C (PKC) [ 38 , 41 ], all of which are consistent with the properties of the basolateral K + channels in animal proximal tubule cells [ 1 , 2 , 42 ].…”

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

“…It was reported that two proinflammatory cytokines, IFN- γ [ 36 , 37 ] and IL-1 β [ 36 , 38 ], affected the activity of the 40 pS K + channel in RPTECs. IFN- γ possessed a time-dependent biphasic effect on the 40 pS K + channel: a delayed suppressive effect and an acute stimulatory one [ 36 , 37 ].…”

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

“…IL-1 β also acutely affected the activity of the 40 pS K + channel in RPTECs and the mode of action was suppressive [ 36 , 38 ]. The effect of IL-1 β was highly likely receptor mediated, since the IL-1 receptor antagonist (IL-1RA) completely abolished it [ 38 ]. With regard to the existence of IL-1 receptors in the kidney, it was reported that the type I IL-1 receptors were widely distributed in renal tubules, as well as glomeruli [ 25 ].…”

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

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Proinflammatory Cytokines and Potassium Channels in the Kidney

Nakamura

Hayashi

Kubokawa

2015

Mediators of Inflammation

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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.

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Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

Section: Effects Of Cytokines On K + Channementioning

confidence: 99%

See 3 more Smart Citations

Proinflammatory Cytokines and Potassium Channels in the Kidney

Nakamura

Hayashi

Kubokawa

2015

Mediators of Inflammation

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Serum Cytokine Alterations Associated with Age of Patients with Nephropathia Epidemica

Shakirova

Khaertynova

Markelova

et al. 2022

BioMed Research International

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Nephropathia epidemica (NE) is a zoonotic disease caused by hantaviruses transmitted from rodents, endemic in the Republic of Tatarstan, Russia. The disease presents clinically with mild, moderate, and severe forms, and time-dependent febrile, oliguric, and polyuric stages of the disease are also recognized. The patient’s cytokine responses have been suggested to play a central role in disease pathogenesis; however, little is known about the different patterns of cytokine expression in NE in cohorts of different ages and sexes. Serum samples and clinical records were collected from 139 patients and 57 controls (healthy donors) and were used to analyze 48 analytes with the Bio-Plex multiplex magnetic bead-based antibody detection kits. Principal component analysis of 137 patient and 55 controls (for which there was full data) identified two components that individually accounted for >15% of the total variance in results and together for 38% of the total variance. PC1 represented a proinflammatory TH17/TH2 cell antiviral cytokine profile and PC2 a more antiviral cytokine profile with patients tending to display one or the other of these. Severity of disease and stage of illness did not show any correlation with PC1 profiles; however, significant differences were seen in patients with high PC1 profiles vs. lower for a number of individual clinical parameters: High PC1 patients showed a reduced number of febrile days, but higher maximum urine output, higher creatinine levels, and lower platelet levels. Overall, the results of this study point towards a stronger proinflammatory profile occurring in younger NE patients, this being associated with markers of acute kidney injury and low levels of high-density cholesterol. This is consistent with previous work indicating that the pathology of NE is immune driven, with an inflammatory immune response being associated with disease and that this immune response is more extreme in younger patients.

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Characteristics and Pharmacological Regulation of Epithelial Na+ Channel (ENaC) and Epithelial Na+ Transport

Marunaka

2014

J Pharmacol Sci

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Abstract. Epithelial Na + transport participates in control of various body functions and conditions: e.g., homeostasis of body fluid content influencing blood pressure, control of amounts of fluids covering the apical surface of alveolar epithelial cells at appropriate levels for normal gas exchange, and prevention of bacterial/viral infection. Epithelial Na + transport via the transcellular pathway is mediated by the entry step of Na + across the apical membrane via Epithelial Na + Channel (ENaC) located at the apical membrane, and the extrusion step of Na + across the basolateral membrane via the Na + ,K + -ATPase located at the basolateral membrane. The ratelimiting step of the epithelial Na + transport via the transcellular pathway is generally recognized to be the entry step of Na + across the apical membrane via ENaC. Thus, up-/down-regulation of ENaC essentially participates in regulatory systems of blood pressure and normal gas exchange. Amount of ENaC-mediated Na + transport is determined by the number of ENaCs located at the apical membrane, activity (open probability) of individual ENaC located at the apical membrane, single channel conductance of ENaC located at the apical membrane, and driving force for the Na + entry via ENaCs across the apical membrane. In the present review article, I discuss the characteristics of ENaC and how these factors are regulated.

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Interleukin-1β suppresses activity of an inwardly rectifying K+ channel in human renal proximal tubule cells

Cited by 3 publications

References 42 publications

Proinflammatory Cytokines and Potassium Channels in the Kidney

Proinflammatory Cytokines and Potassium Channels in the Kidney

Serum Cytokine Alterations Associated with Age of Patients with Nephropathia Epidemica

Characteristics and Pharmacological Regulation of Epithelial Na+ Channel (ENaC) and Epithelial Na+ Transport

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