scholarly journals Differential expression of epithelial sodium channels in human RCC associated with the prognosis and tumor stage: Evidence from integrate analysis

2020 ◽  
Vol 11 (24) ◽  
pp. 7348-7356
Author(s):  
Shangfan Liao ◽  
Huaibin Huang ◽  
Fabiao Zhang ◽  
Dongming Lu ◽  
Shuchao Ye ◽  
...  
Keyword(s):  
Differential Expression ◽  
Sodium Channels ◽  
Tumor Stage ◽  
Epithelial Sodium Channels ◽  
Integrate Analysis

Medullary epithelial sodium channels (ENAC) participate in cerebral blood flow (CBF) autoregulation

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S190-S190
Author(s):  
Eugene Golanov ◽  
Heather Drummond ◽  
Jasleen Shant ◽  
Benjamin Clower ◽  
Betty Chen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sodium Channels ◽  
Epithelial Sodium Channels

scholarly journals The Plant-Derived Glucocorticoid Receptor Agonist Endiandrin A Acts as Co-Stimulator of Colonic Epithelial Sodium Channels (ENaC) via SGK-1 and MAPKs

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49426 ◽  
Author(s):  
Dana Kuntzsch ◽  
Theresa Bergann ◽  
Petra Dames ◽  
Anja Fromm ◽  
Michael Fromm ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Sodium Channels ◽  
Receptor Agonist ◽  
Epithelial Sodium Channels

scholarly journals Proteolytic Regulation of Epithelial Sodium Channels by Urokinase Plasminogen Activator

2015 ◽  
Vol 290 (9) ◽  
pp. 5241-5255 ◽  
Author(s):  
Hong-Long Ji ◽  
Runzhen Zhao ◽  
Andrey A. Komissarov ◽  
Yongchang Chang ◽  
Yongfeng Liu ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Sodium Channels ◽  
Urokinase Plasminogen Activator ◽  
Epithelial Sodium Channels

scholarly journals Ethanol Alters Alveolar Fluid Balance via Nadph Oxidase (NOX) Signaling to Epithelial Sodium Channels (ENaC) in the Lung

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54750 ◽  
Author(s):  
Charles A. Downs ◽  
David Q. Trac ◽  
Lisa H. Kreiner ◽  
Amity F. Eaton ◽  
Nicholle M. Johnson ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Sodium Channels ◽  
Fluid Balance ◽  
Epithelial Sodium Channels

Possible Involvement of Phosphorylation/Dephosphorylation in the Regulation of Epithelial Sodium Channels

1987 ◽  
pp. 261-267
Author(s):  
David S. Lester ◽  
Carol Asher ◽  
Haim Garty
Keyword(s):  
Sodium Channels ◽  
Epithelial Sodium Channels

scholarly journals Epithelial Sodium Channels in Pulmonary Epithelial Progenitor and Stem Cells

2016 ◽  
Vol 12 (9) ◽  
pp. 1150-1154 ◽  
Author(s):  
Yang Liu ◽  
Bi-Jie Jiang ◽  
Run-Zhen Zhao ◽  
Hong-Long Ji
Keyword(s):  
Stem Cells ◽  
Sodium Channels ◽  
Epithelial Sodium Channels

scholarly journals Plasmin improves oedematous blood-gas barrier by cleaving epithelial sodium channels

2020 ◽  
Author(s):  
Runzhen Zhao ◽  
Gibran Ali ◽  
Hong-Guang Nie ◽  
Yongchang Chang ◽  
Deepa Bhattarai ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Sodium Channels ◽  
List Type ◽  
Cleavage Sites ◽  
Blood Gas ◽  
Alveolar Fluid Clearance ◽  
Epithelial Sodium Channels ◽  
Lung Oedema ◽  
Human Lungs ◽  
Oedema Fluid

ABSTRACTBackground and PurposeLung oedema in association with suppressed fibrinolysis is a hallmark of lung injury. We aimed to test whether plasmin cleaves epithelial sodium channels (ENaC) to resolve lung oedema fluid.Experimental ApproachesHuman lungs and airway acid-instilled mice were used for analysing fluid resolution. In silico prediction, mutagenesis, Xenopus oocytes, immunoblotting, voltage clamp, mass spectrometry, protein docking, and alveolar fluid clearance were combined for identifying plasmin specific cleavage sites and benefits.Key ResultsPlasmin led to a marked increment in lung fluid resolution in both human lungs ex vivo and injured mice. Plasmin specifically activated αβγENaC channels in oocytes in a time-dependent manner. Deletion of four consensus proteolysis tracts (αΔ432-444, γΔ131-138, γΔ178-193, and γΔ410-422) eliminated plasmin-induced activation significantly. Further, immunoblotting assays identified 7 cleavage sites (K126, R135, K136, R153, K168, R178, K179) for plasmin to trim both furin-cleaved C-terminal fragments and full-length human γENaC proteins. In addition to confirming the 7 cleavage sites, 9 new sites (R122, R137, R138, K150, K170, R172, R180, K181, K189) in synthesized peptides were found to be cleaved by plasmin with mass spectrometry. These cleavage sites were located in the finger and the thumb, particularly the GRIP domain of human ENaC 3D model composed of two proteolytic centres for plasmin. Novel uncleaved sites beyond the GRIP domain in both α and γ subunits were identified to interrupt the plasmin cleavage-induced conformational change in ENaC channel complexes. Additionally, plasmin could regulate ENaC activity via the G protein signal.Conclusion and ImplicationsWe demonstrate that plasmin could cleave ENaC to benefit the blood-gas exchange by resolving oedema fluid as a potent fibrinolytic therapy for oedematous pulmonary diseases.Bullet point summaryWhat is already knowSerine proteases proteolytically cleave epithelial sodium channels, including plasmin and uPA acutely.Activity of epithelial sodium channels is increased post proteolysis.What this study addsPlasmin cleaves up to 16 sites composed of two proteolytic centres in both full-length and furin-cleaved human γ subunit of epithelial sodium channels in hours.Non-proteolytic sites in both α and γ subunits interrupt the plasmin cleavage-induced channel gating.Intratracheally instilled plasmin facilitates alveolar fluid clearance in normal human and injured mouse lungs.Clinical significanceActivation of human lung epithelial sodium channels by plasmin may benefit lung oedema resolution as a novel therapy for ARDS.

scholarly journals Steroid regulation of epithelial sodium channels (ENaC) in mammary epithelial cells

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Cary R Boyd ◽  
Aniko Naray‐Fejes‐Toth
Keyword(s):  
Epithelial Cells ◽  
Sodium Channels ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Epithelial Sodium Channels ◽  
Steroid Regulation

Abstract 072: Brain Epithelial Sodium Channels on Organum Vasculosum of the Lamina Terminalis Neurons Mediate Sympathoexcitatory Pressor Responses and Neuronal Excitation by Hypertonic NaCl

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Brian J Kinsman ◽  
Kirsteen N Browning ◽  
Sean D Stocker
Keyword(s):  
Sodium Channels ◽  
Salt Intake ◽  
Lamina Terminalis ◽  
Dietary Salt ◽  
Epithelial Sodium Channels ◽  
Adult Rats ◽  
Neuronal Excitation ◽  
Arterial Blood ◽  
Organum Vasculosum

High dietary salt intake raises cerebrospinal fluid (CSF) [Na + ] in salt sensitive subjects to elevate sympathetic nerve activity (SNA), and arterial blood pressure (ABP). This occurs through excitation of NaCl-sensitive sites in the brain, including the organum vasculosum of the lamina terminalis (OVLT). Intriguingly, intracerebroventricular (ICV) pretreatment with benzamil (a non-voltage gated Na + channel blocker) also attenuates those systemic responses to central NaCl. Thus, I hypothesized that benzamil acts on NaCl-sensitive OVLT neurons to attenuate neuronal excitation and elevated SNA and ABP in response to hypertonic NaCl. To evaluate this hypothesis, lumbar SNA and ABP were measured in anesthetized adult rats in response to ICV infusion of 0.15, 0.5, and 1.0 M NaCl with and without prior OVLT microinjection of benzamil (5nmol per 20nL). ICV infusion of NaCl produced concentration-dependent increases in lumbar SNA (0.15M: 101±3%, 0.5M: 118±3%, 1.0M: 130±9% n=4 per group, P<0.05) and mean ABP (0.15M: 1±1mmHg; 0.5M: 5±1mmHg, 1.0M: 12±2mmHg). OVLT microinjection of benzamil significantly attenuated the increase in lumbar SNA (0.15M: 100±2%, 0.5M: 108±2%, 1.0M: 115±3% n=4 per group, P<0.05) and mean ABP (0.15M: 1±0mmHg; 0.5M: 2±1mmHg, 1.0M: 6±2mmHg). In a parallel set of experiments, in vitro whole-cell recordings of OVLT neurons in slices were performed to assess whether blockade of epithelial sodium channels (ENaC) attenuated NaCl-induced excitation. Bath application of +7.5mM NaCl increase action potential (AP) discharge of OVLT neurons (n=11) from 0.46±0.16 Hz to 1.09±0.26 Hz (P<0.05). Subsequent addition of an ENaC selective concentration of benzamil (0.5μM) reversed AP discharge (0.75±0.24 Hz, P<0.05). Isotonic 0.5μM benzamil did not significantly change NaCl-sensitive OVLT neuron (n=13) AP discharge from baseline (0.54±0.14 Hz to 0.60±0.16 Hz, P>0.05). Collectively, this data indicates that elevations in CSF NaCl concentrations excite OVLT neurons via ENaC to elevate SNA and ABP.

ATP masks stretch activation of epithelial sodium channels in A6 distal nephron cells

2002 ◽  
Vol 282 (3) ◽  
pp. F501-F505 ◽  
Author(s):  
He-Ping Ma ◽  
Li Li ◽  
Zhen-Hong Zhou ◽  
Douglas C. Eaton ◽  
David G. Warnock
Keyword(s):  
Patch Clamp ◽  
Sodium Channel ◽  
Sodium Channels ◽  
Mechanical Stretch ◽  
Stretch Activation ◽  
Distal Nephron ◽  
Epithelial Sodium Channels ◽  
Open Probability ◽  
The Mean ◽  
Epithelial Sodium Channel Enac

The mechanosensitivity of the epithelial sodium channel (ENaC) is controversial. Using cell-attached patch-clamp techniques, we found that mechanical stretch stimulated ENaC in A6 distal nephron cells in only three of nine cell-attached patches. However, stretch consistently activated ENaC after apical ATP was scavenged with apical hexokinase plus glucose or after P2receptors in the patch were blocked. The mean open probability ( P o) of ENaC was increased from 0.31 ± 0.04 to 0.61 ± 0.06 ( P < 0.001; n = 9) when patch pipettes contained hexokinase and glucose, or from 0.24 ± 0.05 to 0.55 ± 0.11 ( P < 0.01; n = 7) when patch pipettes contained suramin, respectively. A poorly hydrolyzable ATP analog, ATPγS, in the patch pipettes inhibited ENaC, reducing the P o from 0.41 ± 0.06 to 0.19 ± 0.05 ( P < 0.01; n = 8). Pretreatment of A6 cells with the phospholipase C (PLC) inhibitor U-73122 abolished the effect of ATP on ENaC activity. These data together suggest that ATP, acting through a PLC-dependent purinergic pathway, masks stretch-induced ENaC activation.

Sign in / Sign up

Export Citation Format

Share Document