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. 2009 Oct;20(10):2162–2170. doi: 10.1681/ASN.2008121232

Figure 2.

Figure 2.

Effect of the loss of SHP on fibrotic gene expression and renal fibrosis in the UUO model. (A) Representative RT-PCR analysis of PAI-1, type I collagen, and fibronectin expression in kidneys of SHP−/− mice. RT-PCR was performed on RNA from three different wild-type (WT) mouse kidneys or SHP−/− mouse kidneys. (B) Quantification of RT-PCR results expressed as the mean ± SEM of three independent experiments (n = 9 in each group). β-actin mRNA levels were analyzed as an internal control. **P < 0.01 and #P < 0.05 compared with WT mice. (C) Representative Western blot analysis of PAI-1 and α-SMA expression in the kidneys of SHP−/− mice. (D) Quantification of Western blot results expressed as the mean ± SEM of three independent experiments (n = 9 in each group). β-actin mRNA levels were analyzed as an internal control. **P < 0.01 compared with WT mice. (E and G) Representative kidney tissue sections stained with Sirius red and Masson's trichrome. Magnification, ×200. (a) A normal kidney from a WT mouse. (b) A normal kidney from an SHP knockout (KO) mouse. (c) A UUO kidney from WT mouse at 7 d. (d) A UUO kidney from KO mouse at 7 d. (e) A UUO kidney from WT mouse at 14 d. (f) A UUO kidney from KO mouse at 14 d. (F and H) Computer-based morphometric analysis of kidney fibrosis in the UUO model. Data are the mean ± SEM of five independent measurements (n = 5 in each group). **P < 0.01, *P < 0.001, and #P < 0.05.