1. Targeted deletion of kidney glucose-6 phosphatase leads to nephropathy
Julie Clar, Blandine Gri, Julien Calderaro, Marie-Christine Birling, Yann Hérault, G. Peter A. Smit, Gilles Mithieux, Fabienne Rajas 
Kidney International 
Volume 86, Issue 4, Pages (October 2014)
DOI: /ki
Copyright © 2014 International Society of Nephrology Terms and Conditions

2. Figure 1
Partial deletion of renal G6pc in K-G6pc–/– mice. (a) Kidney-specific excision of G6pc exon 3. Genomic PCR analysis of purified DNA from the kidney, liver, intestine, testis, and epididymis revealed products of 1189, 1029, and 595bp corresponding to the floxed, WT, and excised G6pc alleles, respectively. Specific primers were used to amplify a 320-bp Cre fragment in K-G6pc–/– mice. (b) Renal G6Pase activity in WT (white bar) and K-G6pc–/– (black bar) mice after 6h of fasting. The results are expressed as the mean±s.e.m. (n=12 mice per group). The top panel shows western blot analysis of G6PC in WT and K-G6pc–/– kidney homogenates. (c, d) Immunohistochemical analyses of G6PC in the kidneys of WT mice (c, e) and K-G6pc–/– mice (d, f). DC, distal convoluted tubules; G, glomeruli; PC, proximal convoluted tubules; WT, wild type.
Kidney International  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions

3. Figure 2
Nephromegaly and renal glycogen storage in K-G6pc–/– mice. (a) Kidneys of WT and K-G6pc–/– mice. (b) The weight of two kidneys, (c) the relative weight of the kidneys compared with body mass and (f) renal glycogen content in WT (white bars) and K-G6pc–/– (black bars) mice. (d–e) PAS-stained kidney from WT (d) and K-G6pc–/– mice (e). Data were obtained from mice after 6h of fasting and are expressed as the mean±s.e.m. (n=12 mice per group). Significant differences between WT and K-G6pc–/– mice are indicated (***P<0.001). DC, distal convoluted tubules; G, glomeruli; PC, proximal convoluted tubules; WT, wild type.
Kidney International  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions

4. Figure 3
Morphological alterations and podocyte damage in K-G6pc–/– kidneys. Histological analyses of hematoxylin-eosin staining from WT (a, c) and K-G6pc–/– kidneys (b, d). (c, d) Correspond to a higher magnification of the kidney cortex observed in a and b, respectively. (e) Expression of podocyte marker proteins in the kidneys of WT (white bars) and K-G6pc–/– (black bars) mice. Nphs2: Podocin, Synpo: Synaptopodin, Podxl: Podocalyxin. The mRNA levels are expressed as a ratio relative to the Rpl19 mRNA level. The results are expressed as the mean±s.e.m. (n=5 mice per group). Significant differences between WT and K-G6pc–/– mice are indicated (**P<0.01 and ***P<0.001). On the right of e are western blot analyses of Nephrin, NPHS2, and GAPDH (control) proteins in WT and K-G6pc–/– kidney homogenates. DC, distal convoluted tubules; G, glomeruli; PC, proximal convoluted tubules; WT, wild type.
Kidney International  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions

5. Figure 4
Activation of the renin–angiotensin system leading to epithelial–mesenchymal transition and inflammation in K-G6pc–/– kidneys. (a, b) The expression of renin–angiotensin system components (a) and of factors involved in epithelial–mesenchymal transition (b) was analyzed in the kidneys of WT (white bars) and K-G6pc–/– (black bars) mice. On the right of b are western blot analyses of E-cadherin, β1-catenin, Vimentin, and GAPDH (control) proteins in WT and K-G6pc–/– kidney homogenates. (c–f) Electron microscopic analyses of glomeruli (c, d) and proximal convoluted tubules (e, f) of WT (C and E) and K-G6pc–/– kidneys (d, f). (g) Determination of inflammation in the kidneys of WT (white bars) and K-G6pc–/– (black bars) mice. The mRNA levels are expressed as a ratio relative to the Rpl19 mRNA level. The results are expressed as the mean±s.e.m. (n=5 mice per group). Significant differences between WT and K-G6pc–/– mice are indicated (**P<0.01). Agt, angiotensinogen; aSMA, α2 smooth muscle actin; Cdh1, E-cadherin; Ctnnb1, catenin β1; PAI1, plasminogen activator inhibitor type 1; Tgfb1, transforming growth factor β1; Tnf, tumor necrosis factor; WT, wild type; ZO1, tight junction protein ZO-1.
Kidney International  , DOI: ( /ki )
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6. Figure 5
Altered renal lipid metabolism and lipid deposits in K-G6pc–/– kidneys. Histological analysis of Sudan red staining from WT (a) and K-G6pc–/– kidneys (b–c). (c) Corresponds to a higher magnification of the lipid deposits showed in b. (d) Expression of the main lipogenic genes in the kidneys of WT (white bars) and K-G6pc–/– (black bars) mice. The mRNA levels are expressed as a ratio relative to the Rpl19 mRNA level. The results are expressed as the mean±s.e.m. (n=5 mice per group). Significant differences between WT and K-G6pc–/– mice are indicated (**P<0.01). Acaca, acetyl-coenzyme A carboxylase α; Chrebp, carbohydrate-responsive element-binding protein; Fasn, fatty acid synthase; Hmgcr, 3-hydroxy-3-methylglutaryl coenzyme A reductase; Hmgcs2, 3-hydroxy-3-methylglutaryl coenzyme A synthase 2; Scd1, stearoyl-coenzyme A desaturase 1; Srebf1, sterol regulatory element-binding factor 1; Srebf2, sterol regulatory element-binding factor 2; WT, wild type.
Kidney International  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions