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Epithelial sodium channels (ENaC) produce extracellular positive DC potentials in the retinal neuroepithelium.

ABSTRACT: Positive DC (direct current) potentials were measured in the extracellular space in the retinal neuroepithelium of chick embryos. The positive DC potential was suppressed by amiloride, a blocker for epithelial Na(+) channels (ENaC). Amiloride also decreased the resistance of the extracellular space as measured by passing a constant current through a microelectrode. The positive DC potential is necessary for the guidance of retinal ganglion cell axons [1].

SUBMITTER: Yamashita M

PROVIDER: S-EPMC4707180 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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Epithelial sodium channels (ENaC) produce extracellular positive DC potentials in the retinal neuroepithelium.

Yamashita Masayuki M

Data in brief 20151214

Positive DC (direct current) potentials were measured in the extracellular space in the retinal neuroepithelium of chick embryos. The positive DC potential was suppressed by amiloride, a blocker for epithelial Na(+) channels (ENaC). Amiloride also decreased the resistance of the extracellular space as measured by passing a constant current through a microelectrode. The positive DC potential is necessary for the guidance of retinal ganglion cell axons [1]. ...[more]

PMID: 26862567

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Project description:BackgroundSalt sensitivity of blood pressure is an independent predictor of cardiovascular morbidity and mortality. The exact mechanism by which salt intake increases blood pressure and cardiovascular risk is unknown. We previously found that sodium entry into antigen-presenting cells (APCs) via the amiloride-sensitive epithelial sodium channel EnaC (epithelial sodium channel) leads to the formation of IsoLGs (isolevuglandins) and release of proinflammatory cytokines to activate T cells and modulate salt-sensitive hypertension. In the current study, we hypothesized that ENaC-dependent entry of sodium into APCs activates the NLRP3 (NOD [nucleotide-binding and oligomerization domain]-like receptor family pyrin domain containing 3) inflammasome via IsoLG formation leading to salt-sensitive hypertension.MethodsWe performed RNA sequencing on human monocytes treated with elevated sodium in vitro and Cellular Indexing of Transcriptomes and Epitopes by Sequencing analysis of peripheral blood mononuclear cells from participants rigorously phenotyped for salt sensitivity of blood pressure using an established inpatient protocol. To determine mechanisms, we analyzed inflammasome activation in mouse models of deoxycorticosterone acetate salt-induced hypertension as well as salt-sensitive mice with ENaC inhibition or expression, IsoLG scavenging, and adoptive transfer of wild-type dendritic cells into NLRP3 deficient mice.ResultsWe found that high levels of salt exposure upregulates the NLRP3 inflammasome, pyroptotic and apoptotic caspases, and IL (interleukin)-1β transcription in human monocytes. Cellular Indexing of Transcriptomes and Epitopes by Sequencing revealed that components of the NLRP3 inflammasome and activation marker IL-1β dynamically vary with changes in salt loading/depletion. Mechanistically, we found that sodium-induced activation of the NLRP3 inflammasome is ENaC and IsoLG dependent. NLRP3 deficient mice develop a blunted hypertensive response to elevated sodium, and this is restored by the adoptive transfer of NLRP3 replete APCs.ConclusionsThese findings reveal a mechanistic link between ENaC, inflammation, and salt-sensitive hypertension involving NLRP3 inflammasome activation in APCs. APC activation via the NLRP3 inflammasome can serve as a potential diagnostic biomarker for salt sensitivity of blood pressure.

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Epithelial sodium channels (ENaC) produce extracellular positive DC potentials in the retinal neuroepithelium.

Publications

Epithelial sodium channels (ENaC) produce extracellular positive DC potentials in the retinal neuroepithelium.

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