Adiponectin regulates AQP3 via PPARα in human hepatic stellate cells.

Biochem Biophys Res Commun

Hans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology & Hepatology, Internal Medicine III, Medical University of Vienna, Austria. Electronic address:

Published: August 2017

Aquaporins (AQPs) are trans-membrane proteins which allow the movement of water and glycerol required by hepatic stellate cells (HSC) for triglyceride formation and lipid storage. Adiponectin (ADPQ) is a hormone produced by the adipose tissue, which is known to increase AQP3 expression. Since ADPQ receptor signals via the nuclear receptor PPAR we aimed to explore the role of this pathway in AQP3 regulation by ADPQ in HSC. AQP3 and CPT1α expression increased only after ADPQ but not rosiglitazone stimulation. In LX2 cells co-transfected with plasmids expressing PPARα or PPARγ coupled to a luciferase reporter gene, only PPARα increased luciferase activity after ADPQ stimulation. Collectively, our findings demonstrate that ADPQ increases AQP3 expression through PPARα-mediated signaling in HSC.

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http://dx.doi.org/10.1016/j.bbrc.2017.06.009DOI Listing

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