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. 2012 Sep 1;23(17):3370–3379. doi: 10.1091/mbc.E11-12-1010

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© 2012 Wasik et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 4: — Knockdown of septin 7 or alteration of the assembly of septins increases glucose uptake in HIRc cells and podocytes. (A) Septin 7 siRNA leads to 81% reduction in septin 7 expression in HIRc cells. CD2AP expression level remains unchanged in septin 7 knockdown cells. HIRc cells were transfected with rat septin 7 SMARTpool siRNA (septin 7), siCONTROL Non-Targeting Pool siRNA (control), or Lipofectamine 2000 alone (lipof.), and analyzed by immunoblotting 72 h after transfection. Actin is included as a loading control. (B) Depletion of septin 7 increases the glucose uptake activity of HIRc cells by 19% compared with the control siRNA-transfected cells (set to 100%) in basal state. (C) Knockdown of septin 7 increases the glucose uptake activity of HIRc cells by 17% in serum-starved cells (septin 7 siRNA, − insulin) and by 144% after insulin stimulation (septin 7 siRNA, + insulin). The increase in glucose uptake in control siRNA-transfected cells is 90% after insulin stimulation (control siRNA, + insulin). Glucose uptake activity of the control siRNA-transfected and serum-starved cells is set to 100% (control siRNA, − insulin). (D) HIRc cells treated with FCF show 131% increase in glucose uptake activity in basal state compared with solvent only–treated cells (DMSO, set to 100%). (E) FCF treatment increases the glucose uptake activity of HIRc cells by 41% in serum-starved cells (FCF, − insulin) and by 198% after insulin stimulation (FCF, + insulin). The increase in glucose uptake in solvent only–treated cells is 64% after insulin stimulation (DMSO, + insulin). Glucose uptake activity of the solvent only–treated and serum-starved cells is set to 100% (DMSO, − insulin). (F) Alteration of septin assembly by FCF in mouse podocytes leads to a 56% increase in glucose uptake in basal state. (G) FCF treatment increases the glucose uptake activity of mouse podocytes by 52% in serum-starved cells (FCF, − insulin) and by 235% after insulin stimulation (FCF, + insulin). Solvent only–treated mouse podocytes show a 27% increase in glucose uptake after insulin stimulation (DMSO, + insulin). HIRC cells were transfected with septin-7 siRNA (A–C) or treated with 50 μM FCF (D and E), and glucose uptake was measured as described in Materials and Methods in basal state (B and D) or after serum starvation (−) and treatment with 200 nM insulin (+) (C and E). Mouse podocytes were treated with 50 μM FCF for 4 h (F and G) and treated (+) or not (−) with 20 nM insulin (G). Bars show the mean and error bars show the SD of three independent experiments using Student's t test.