Endophilin A2 Influences Volume-Regulated Chloride Current by Mediating ClC-3 Trafficking in Vascular Smooth Muscle Cells.
Circ J
; 80(11): 2397-2406, 2016 Oct 25.
Article
en En
| MEDLINE
| ID: mdl-27760895
BACKGROUND: Previous research has demonstrated that ClC-3 is responsible for volume-regulated Cl-current (ICl.vol) in vascular smooth muscle cells (VSMCs). However, it is still not clear whether and how ClC-3 is transported to cell membranes, resulting in alteration ofICl.vol.MethodsâandâResults:Volume-regulated chloride current (ICl.vol) was recorded by whole-cell patch clamp recording, and Western blotting and co-immunoprecipitation were performed to examine protein expression and protein-protein interaction. Live cell imaging was used to observe ClC-3 transporting. The results showed that an overexpression of endophilin A2 could increaseICl.vol, while endophilin A2 knockdown decreasedICl.vol. In addition, the SH3 domain of endophilin A2 mediated its interaction with ClC-3 and promotes ClC-3 transportation from the cytoplasm to cell membranes. The regulation of ClC-3 channel activity was also verified in basilar arterial smooth muscle cells (BASMCs) isolated from endophilin A2 transgenic mice. Moreover, endophilin A2 increase VSMCs proliferation induced by endothelin-1 or hypo-osmolarity. CONCLUSIONS: The present study identified endophilin A2 as a ClC-3 channel partner, which serves as a new ClC-3 trafficking insight in regulatingICl.volin VSMCs. This study provides a new mechanism by which endophilin A2 regulates ClC-3 channel activity, and sheds light on how ClC-3 is transported to cell membranes to play its critical role as a chloride channel in VSMCs function, which may be involved in cardiovascular diseases. (Circ J 2016; 80: 2397-2406).
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Aciltransferasas
/
Membrana Celular
/
Cloruros
/
Canales de Cloruro
/
Miocitos del Músculo Liso
/
Potenciales de la Membrana
/
Músculo Liso Vascular
Límite:
Animals
Idioma:
En
Revista:
Circ J
Asunto de la revista:
ANGIOLOGIA
/
CARDIOLOGIA
Año:
2016
Tipo del documento:
Article
Pais de publicación:
Japón