Netrin-1 Promotes Epithelial Sodium Channel-Mediated Alveolar Fluid Clearance via Activation of the Adenosine 2B Receptor in Lipopolysaccharide-Induced Acute Lung Injury | Zendy

Jing He | Zendy; Yan Zhao | Zendy; Wang Deng | Zendy; Daoxin Wang | Zendy

Open Access

Netrin-1 Promotes Epithelial Sodium Channel-Mediated Alveolar Fluid Clearance via Activation of the Adenosine 2B Receptor in Lipopolysaccharide-Induced Acute Lung Injury

Author(s) -

Jing He,

Yan Zhao,

Wang Deng,

Daoxin Wang

Publication year - 2014

Publication title -

respiration

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.264

H-Index - 81

eISSN - 1423-0356

pISSN - 0025-7931

DOI - 10.1159/000358066

Subject(s) - epithelial sodium channel , medicine , adenosine , bronchoalveolar lavage , cyclic adenosine monophosphate , lung , pulmonary edema , lipopolysaccharide , endocrinology , receptor , pharmacology , sodium , chemistry , organic chemistry

The epithelial sodium channel (ENaC) is the driving force for pulmonary edema absorption in acute lung injury (ALI). Netrin-1 is a newly found anti-inflammatory factor that works by activating the adenosine 2B receptor (A2BAR). Meanwhile, activated A2BAR has the potential to enhance ENaC-dependent alveolar fluid clearance (AFC). However, whether netrin-1 can increase ENaC-mediated AFC by activating A2BAR remains unclear.

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