Journal: Frontiers in Physiology
Article Title: Empagliflozin Contributes to Polyuria via Regulation of Sodium Transporters and Water Channels in Diabetic Rat Kidneys
Figure Lengend Snippet: Empagliflozin causes no significant changes to AQP3 and AQP1 but tends to increase AQP7 level in diabetic rat kidneys. (A) Representative renal sections immunostained with anti-AQP3. (B) Quantitative analysis of results for AQP3 shows no significant change among groups. Magnification, ×200. (C) Representative immunoblot reacting with anti-NCC, anti-α-ENaC and anti- γ-ENaC. (D) Densitometric analysis shows that the expression of AQP3 protein significantly increased in all OLETF rats. Lixisenatide treatment further increased the expression of AQP3. ∗ P
Article Snippet: Membranes were incubated with the following primary antibodies: AQP1 (Alomone Labs, Jerusalem, Israel), AQP2 (Alomone Labs), p261-AQP2 (Novus Biologicals, Littleton, CO, United States), AQP3 (Alomone Labs), AQP7 (Alomone Labs), cyclin-dependent kinase 1 (cdk1; Santa Cruz Biotechnology, Inc., Santa Cruz, CA, United States), cdk5 (Santa Cruz Biotechnology, Inc.), Na+/H+ exchanger isoform 3 (NHE3; StressMarq Biosciences Inc., Victoria, BC, Canada), extracellular signal–regulated kinase (ERK; Cell Signaling Technology, Danvers, MA, United States), p-Erk (Cell Signaling Technology), p -glycogen synthase kinase 3α (pGSK3α; Santa Cruz Biotechnology, Inc.), Na+-Cl- cotransporter (NCC; StressMarq Biosciences), NKCC2 (StressMarq Biosciences), phosphatase 1β (PP1β; Santa Cruz Biotechnology, Inc.), PP2B (Santa Cruz Biotechnology, Inc.), vasopressin V2 receptor (V2R; Alomone Labs), α-epithelial Na+ channel (ENaC; StressMarq Biosciences); γ-ENaC (StressMarq Biosciences), p38 mitogen-activated protein kinase (p38; Cell Signaling Technology), p-p38 (Cell Signaling Technology) and β-actin (Sigma-Aldrich, St. Louis, MO, United States).