scholarly journals Leptin‐Induced Endothelial Dysfunction is Mediated by Endothelial Mineralocorticoid Receptor Epithelial Sodium Channel Activation in Female Mice

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Jessica L. Faulkner ◽  
Simone Kennard ◽  
Iris Jaffe ◽  
Eric J. Belin de Chantemele
Keyword(s):  
Endothelial Dysfunction ◽  
Sodium Channel ◽  
Mineralocorticoid Receptor ◽  
Epithelial Sodium Channel ◽  
Channel Activation ◽  
Female Mice ◽  
Sodium Channel Activation

scholarly journals Endothelial sodium channel activation promotes cardiac stiffness and diastolic dysfunction in Western diet fed female mice

Metabolism ◽  
2020 ◽  
Vol 109 ◽  
pp. 154223 ◽  
Author(s):  
James R. Sowers ◽  
Javad Habibi ◽  
Guanghong Jia ◽  
Brian Bostick ◽  
Camila Manrique-Acevedo ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Sodium Channel ◽  
Western Diet ◽  
Channel Activation ◽  
Female Mice ◽  
Sodium Channel Activation

scholarly journals Azithromycin Inhibits Constitutive Airway Epithelial Sodium Channel Activation in Vitro and Modulates Downstream Pathogenesis in Vivo

2020 ◽  
Vol 43 (4) ◽  
pp. 725-730 ◽  
Author(s):  
Haruka Fujikawa ◽  
Taise Kawakami ◽  
Ryunosuke Nakashima ◽  
Aoi Nasu ◽  
Shunsuke Kamei ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Airway Epithelial ◽  
Channel Activation ◽  
Sodium Channel Activation

Abstract 111: Endothelial Sodium Channel Activation Promotes Angiotensin II Induced Arterial Stiffness and Endothelial Dysfunction

Hypertension ◽  
2018 ◽  
Vol 72 (Suppl_1) ◽  
Author(s):  
Annayya Aroor ◽  
Guanghong Jia ◽  
Michael Hill ◽  
Javad Habibi ◽  
Yan Yang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Arterial Stiffness ◽  
Sodium Channel ◽  
Channel Activation ◽  
Sodium Channel Activation

scholarly journals A Novel Tumor Necrosis Factor–mediated Mechanism of Direct Epithelial Sodium Channel Activation

2014 ◽  
Vol 190 (5) ◽  
pp. 522-532 ◽  
Author(s):  
István Czikora ◽  
Abdel Alli ◽  
Hui-Fang Bao ◽  
David Kaftan ◽  
Supriya Sridhar ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Sodium Channel ◽  
Tumor Necrosis ◽  
Epithelial Sodium Channel ◽  
Channel Activation ◽  
Sodium Channel Activation ◽  
Necrosis Factor

scholarly journals Inter-α-Inhibitor Blocks Epithelial Sodium Channel Activation and Decreases Nasal Potential Differences in ΔF508 Mice

2014 ◽  
Vol 50 (5) ◽  
pp. 953-962 ◽  
Author(s):  
Ahmed Lazrak ◽  
Asta Jurkuvenaite ◽  
Emily C. Ness ◽  
Shaoyan Zhang ◽  
Bradford A. Woodworth ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Channel Activation ◽  
Sodium Channel Activation

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.

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