scholarly journals Pioglitazone‐induced sodium retention in rat is independent of alpha subunit of epithelial sodium channel (ENaCá) expression in distal nephron

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Hongbao Ma ◽  
Bala Ponnam ◽  
Jinping Li ◽  
Shyan‐Yih Chou
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Alpha Subunit ◽  
Sodium Retention ◽  
Distal Nephron

scholarly journals Epithelial Sodium Channel Is a Key Mediator of Growth Hormone-Induced Sodium Retention in Acromegaly

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3294-3305 ◽  
Author(s):  
Peter Kamenicky ◽  
Say Viengchareun ◽  
Anne Blanchard ◽  
Geri Meduri ◽  
Philippe Zizzari ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Sodium Transport ◽  
Epithelial Sodium Channel ◽  
Janus Kinase ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Signal Transducer ◽  
Distal Nephron ◽  
Igf I ◽  
Gc Rats

Acromegalic patients present with volume expansion and arterial hypertension, but the renal sites and molecular mechanisms of direct antinatriuretic action of GH remain unclear. Here, we show that acromegalic GC rats, which are chronically exposed to very high levels of GH, exhibited a decrease of furosemide-induced natriuresis and an increase of amiloride-stimulated natriuresis compared with controls. Enhanced Na+,K+-ATPase activity and altered proteolytic maturation of epithelial sodium channel (ENaC) subunits in the cortical collecting ducts (CCDs) of GC rats provided additional evidence for an increased sodium reabsorption in the late distal nephron under chronic GH excess. In vitro experiments on KC3AC1 cells, a murine CCD cell model, revealed the expression of functional GH receptors and IGF-I receptors coupled to activation of Janus kinase 2/signal transducer and activator of transcription 5, ERK, and AKT signaling pathways. That GH directly controls sodium reabsorption in CCD cells is supported by: 1) stimulation of transepithelial sodium transport inhibited by GH receptor antagonist pegvisomant; 2) induction of α-ENaC mRNA expression; and 3) identification of signal transducer and activator of transcription 5 binding to a response element located in the α-ENaC promoter, indicative of the transcriptional regulation of α-ENaC by GH. Our findings provide the first evidence that GH, in concert with IGF-I, stimulates ENaC-mediated sodium transport in the late distal nephron, accounting for the pathogenesis of sodium retention in acromegaly.

scholarly journals Cathepsin B cleaves and activates the alpha subunit of the epithelial sodium channel

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Abdel A Alli ◽  
John Z Song ◽  
Otor Al-Khalili ◽  
Hui-Fang Bao ◽  
He-Ping Ma ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Cathepsin B ◽  
Epithelial Sodium Channel ◽  
Alpha Subunit

Experimental nephrotic syndrome leads to proteolytic activation of the epithelial sodium channel (ENaC) in the mouse kidney

2021 ◽  
Author(s):  
Bernhard N. Bohnert ◽  
Daniel Essigke ◽  
Andrea Janessa ◽  
Jonas C Schneider ◽  
Matthias Wörn ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Sodium Channel ◽  
Serine Protease ◽  
Cleavage Site ◽  
Mineralocorticoid Receptor ◽  
Epithelial Sodium Channel ◽  
Sodium Retention ◽  
Cleavage Sites ◽  
Proteolytic Activation ◽  
Epithelial Sodium Channel Enac

Proteolytic activation of the renal epithelial sodium channel ENaC involves cleavage events in its α- and γ-subunits and is thought to mediate sodium retention in nephrotic syndrome (NS). However, detection of proteolytically processed ENaC in kidney tissue from nephrotic mice has been elusive so far. We used a refined Western blot technique to reliably discriminate full-length α- and γ-ENaC and their cleavage products after proteolysis at their proximal and distal cleavage sites (designated from the N-terminus), respectively. Proteolytic ENaC activation was investigated in kidneys from mice with experimental NS induced by doxorubicin or inducible podocin deficiency with or without treatment with the serine protease inhibitor aprotinin. Nephrotic mice developed sodium retention and increased expression of fragments of α- and γ-ENaC cleaved at both the proximal and more prominently at the distal cleavage site, respectively. Treatment with aprotinin but not with the mineralocorticoid receptor antagonist canrenoate prevented sodium retention and upregulation of the cleavage products in nephrotic mice. Increased expression of cleavage products of α- and γ-ENaC was similarly found in healthy mice treated with a low salt diet, sensitive to mineralocorticoid receptor blockade. In human nephrectomy specimens, γ-ENaC was found in the full-length form and predominantly cleaved at its distal cleavage site. In conclusion, murine experimental NS leads to aprotinin-sensitive proteolytic activation of ENaC at both proximal and more prominently distal cleavage sites of its α- and γ-subunit, most likely by urinary serine protease activity or proteasuria.

scholarly journals Expression and purification of the alpha subunit of the epithelial sodium channel, ENaC

2016 ◽  
Vol 117 ◽  
pp. 67-75
Author(s):  
Bharat G. Reddy ◽  
Qun Dai ◽  
Carmel M. McNicholas ◽  
Catherine M. Fuller ◽  
John C. Kappes ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Alpha Subunit ◽  
Expression And Purification ◽  
Epithelial Sodium Channel Enac

scholarly journals A long isoform of the epithelial sodium channel alpha subunit forms a highly active channel

Channels ◽  
2015 ◽  
Vol 9 (1) ◽  
pp. 30-43 ◽  
Author(s):  
Jonathan M Berman ◽  
Cristin Brand ◽  
Mouhamed S Awayda
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Alpha Subunit ◽  
Highly Active ◽  
Active Channel

scholarly journals Evaluation of gene SCNN1A responsible for the synthesis of alpha subunit of epithelial sodium channel in transient tachypnea of newborn

2013 ◽  
Vol 48 (1) ◽  
pp. 35-39 ◽  
Author(s):  
Osman Oztekin ◽  
Mahmut Akyol ◽  
Salih Kalay ◽  
Gonul Tezel ◽  
Mustafa Akcakus ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Alpha Subunit
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