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Results: 7

1.
Figure 3.

Figure 3. From: Glcci1 Deficiency Leads to Proteinuria.

GLCCI1 is expressed in capillary state but insignificantly in earlier S-shape glomeruli. Immunostaining of GLCCI1 in fetal mouse kidney shows expression at embryonic day 15.5. GLCCI1 is initially expressed in podocyte cytoplasm (arrowheads) of capillary loop stage glomerulus. At the earlier S-shape stage (asterisk), GLCCI1 expression is insignificant.

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.
2.
Figure 4.

Figure 4. From: Glcci1 Deficiency Leads to Proteinuria.

Dexamethasone induces expression of Glcci1 in mouse podocytes and glomeruli. RT-PCR for Glcci1 and β-actin (internal standard) expression was carried out on total RNA isolated from DEX-treated cultured mouse podocytes and glomeruli isolated from mice treated with DEX. (A) Podocytes were cultured at different DEX concentrations, and in one case with the GR antagonist RU486 for 30 minutes before the addition of DEX. (B) Expression in glomeruli isolated from mice treated with DEX (2 mg/kg) for 12 hours. Histograms show an increase in Glcci1 expression after DEX treatment.

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.
3.
Figure 1.

Figure 1. From: Glcci1 Deficiency Leads to Proteinuria.

Expression of Glcci1 in mouse organs reveals varying tissue expression and strong upregulation in kidney glomeruli. (A) Using RT-PCR, high expression is seen in testis, brain, and thymus; somewhat lower expression is seen in lymph nodes, spleen, and eye; and weak signals are seen in lung, heart, liver, muscle, uterus, and whole kidney. However, RT-PCR of RNA from isolated glomeruli gives a strong signal compared with that in RNA from the rest of the kidney. (B) Northern blot reveals strong expression of mRNAs of 5.0 and 6.0 kb in the thymus and of about 2.0-kb-size mRNA in testis. The other organs reveal weak signals for both the 2.0- and 6.0-kb mRNAs. (C) Western blotting of protein extracted from isolated glomeruli show a strong single band of about 60 kD and a weak staining of same size protein in the rest of the kidney.

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.
4.
Figure 5.

Figure 5. From: Glcci1 Deficiency Leads to Proteinuria.

GLCCI1 is expressed in podocytes and mesangial cells in the zebrafish pronephros. (A) RT-PCR was performed on total embryonic RNA at 3, 6, 9, and 12 hpf, and at days 1 to 7 postfertilization. glcci1 mRNA is detected in whole zebrafish embryos. β-actin is a housekeeping gene known to be expressed in early development of zebrafish. (B) Immunohistochemistry shows negative staining for Glcci1 in the glomerulus with control rabbit IgG. (C) Immunohistochemistry shows positive staining for Glcci1 expression in the zebrafish pronephros (arrowheads) (original magnification, ×20). (D) At higher magnification, immunostaining of cytoplasm and a mesangium-like pattern are visible. (E) RT-PCR of RNA isolated from single zebrafish embryo glomeruli demonstrates distinct expression of glcci1. G, glomeruli; RoF, rest of fish; F, whole zebrafish.

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.
5.
Figure 2.

Figure 2. From: Glcci1 Deficiency Leads to Proteinuria.

Kidney GLCCI1 expression is restricted to podocytes and mesangial cells. Paraffin sections of adult mouse kidney cortex were immunostained with the polyclonal anti-human GLCCI1 antibody or rabbit IgG (5 μg/ ml) as control. (A) No immunoreactivity was observed in adjacent specimens immunostained with normal rabbit IgG. (B) Low power magnification reveals immunoreactivity exclusively in glomeruli of the mouse kidney cortex. (C) At higher magnification, immunostaining of the glomerular podocytes and mesangium with strong cytoplasm staining is apparent. Magnifications: ×100 in overviews and ×800 in single glomeruli. (D) Immunogold labeling in normal mouse capillaries shows the majority of gold particles to be located in the podocyte foot processes. Bars, A and B, 100 μm; C, 10 μm; and D, 0.5 μm.

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.
6.
Figure 7.

Figure 7. From: Glcci1 Deficiency Leads to Proteinuria.

Disruption of glcci1 expression causes abnormal glomerular capillary loops, podocyte effacement, and proteinuria. (A and B) In light microscopy, Periodic acid-Schiff staining shows dilated capillary loops and widened Bowman's space (A) compared with wild type (B). (C and D) In glcci1 knockdown embryos, the foot processes are largely lost because of effacement, but normal areas with intact slit membranes were also observed (C). Ultrastructural studies show normal podocyte foot processes, glomerular basement membrane, and endothelial cells in wild-type embryos (D). (E) Not only nephrin knockdown embryos but also glcci1 knockdown embryos develop proteinuria that can be observed by SDS-PAGE analysis. The main protein penetrating the filtration barrier was identified by mass spectrometry analysis as vitellogenin that has a size of about 150 and 70 kD, of the same size as BSA that primarily appears to be a degradation product of vitellogenin.

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.
7.
Figure 6.

Figure 6. From: Glcci1 Deficiency Leads to Proteinuria.

Disruption of glcci1 expression with splice donor antisense MOs causes pericardial edema, short stature, and curved body axis. The efficacy of the injected MO was compared by RT-PCR. (A) glcci1 MO targeting the exon 2 splice donor caused an insertion of part of intron 2 and a deletion of exon 2. (B) The changes in amplified RNA fragments are seen as a decrease in amplicon size (375 bp versus 530 bp) as illustrated here by amino acid sequences that are aligned in the panel or as a nonsplicing of adjacent intron, visible as an increase in amplicon size (567 bp) caused by a truncation after a stretch of nonsense amino acids. (C) Compared with wild-type embryos, glcci1 MO larvae develop severe cardiac edema and bent tail at 96 hpf. (D) Rescue of the glcci1 MO phenotype with zebrafish glcci1 mRNA coinjection. Coinjection with 100 pg of zebrafish glcci1 mRNA completely rescued the phenotype (97%).

Yukino Nishibori, et al. J Am Soc Nephrol. 2011 November;22(11):2037-2046.

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