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The Prorenin Receptor and its Soluble Form Contribute to Lipid Homeostasis

biorxiv. 2020; 
Eva Gatineau, Gertrude Arthur, Audrey Poupeau, Kellea Nichols, Brett T. Spear, Gregory Graf, Ryan Temel, Frédérique Yiannikouris
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Gene Synthesis Hep-G2 cells (ATCC) were cultured in the presence of Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% (v/v) fetal bovine serum and 1% (v/v) of a mixture of penicillin and streptomycin. PRR was silenced by mouse Stealth RNA interference designed for Atp6ap2 gene (PRR) using lipofectamineTM 2000 (life technology), and according to the procedure recommended by the manufacturer. 3T3-L1 cells were cultured in the presence of DMEM supplemented with 10% (v/v) fetal bovine serum and 1% (v/v) of a mixture of penicillin and streptomycin and treated with mouse recombinant sPRR-HisTag (residues 18–276, Genscript) or with vehicle for 24 hours. Get A Quote

摘要

Obesity is associated with alterations in hepatic lipid metabolism. We previously identified the prorenin receptor (PRR) as a potential contributor to liver steatosis. Therefore, we aimed to determine the relative contribution of PRR and its soluble form, sPRR, to lipid homeostasis. PRR-floxed male mice were treated with an adeno-associated virus with thyroxine-binding globulin promoter driven Cre to delete specifically PRR in hepatocytes (Liver PRR KO mice). Hepatic PRR deletion did not change the body weight but increased liver weights. Liver PRR KO mice exhibited higher plasma cholesterol levels and lower hepatic LDLR protein than control mice. Surprisingly, hepatic PRR deletion elevated hepatic cholesterol,... More

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