A Novel Tumor Necrosis Factor-mediated Mechanism of Direct Epithelial Sodium Channel Activation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F14%3A43887246" target="_blank" >RIV/60076658:12310/14:43887246 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1164/rccm.201405-0833OC" target="_blank" >http://dx.doi.org/10.1164/rccm.201405-0833OC</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1164/rccm.201405-0833OC" target="_blank" >10.1164/rccm.201405-0833OC</a>

Jazyk výsledku

angličtina

Název v původním jazyce

A Novel Tumor Necrosis Factor-mediated Mechanism of Direct Epithelial Sodium Channel Activation

Popis výsledku v původním jazyce

Rationale: Alveolar liquid clearance is regulated by Na+ uptake through the apically expressed epithelial sodium channel (ENaC) and basolaterally localized Na+-K+-ATPase in type II alveolar epithelial cells. Dysfunction of these Na+ transporters during pulmonary inflammation can contribute to pulmonary edema. Objectives: In this study, we sought to determine the precise mechanism by which the TIP peptide, mimicking the lectin-like domain of tumor necrosis factor (TNF), stimulates Na+ uptake in a homologous cell system in the presence or absence of the bacterial toxin pneumolysin (PLY). Methods: We used a combined biochemical, electrophysiological, and molecular biological in vitro approach and assessed the physiological relevance of the lectin-like domain of TNF in alveolar liquid clearance in vivo by generating triple-mutant TNF knock-in mice that express a mutant TNF with deficient Na+ uptake stimulatory activity. Measurements and Main Results: TIP peptide directly activates ENaC, bu

Název v anglickém jazyce

A Novel Tumor Necrosis Factor-mediated Mechanism of Direct Epithelial Sodium Channel Activation

Popis výsledku anglicky

Rationale: Alveolar liquid clearance is regulated by Na+ uptake through the apically expressed epithelial sodium channel (ENaC) and basolaterally localized Na+-K+-ATPase in type II alveolar epithelial cells. Dysfunction of these Na+ transporters during pulmonary inflammation can contribute to pulmonary edema. Objectives: In this study, we sought to determine the precise mechanism by which the TIP peptide, mimicking the lectin-like domain of tumor necrosis factor (TNF), stimulates Na+ uptake in a homologous cell system in the presence or absence of the bacterial toxin pneumolysin (PLY). Methods: We used a combined biochemical, electrophysiological, and molecular biological in vitro approach and assessed the physiological relevance of the lectin-like domain of TNF in alveolar liquid clearance in vivo by generating triple-mutant TNF knock-in mice that express a mutant TNF with deficient Na+ uptake stimulatory activity. Measurements and Main Results: TIP peptide directly activates ENaC, bu

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

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Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE

ISSN

1073-449X

e-ISSN

—

Svazek periodika

190

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

522-532

Kód UT WoS článku

000341554400007

EID výsledku v databázi Scopus

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