Targeted disruption of TGF-β1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction
J. Clin. Invest. Misako Sato, et al. 112:1486 doi:10.1172/JCI19270 [Go to this article.]

Figure 3
Lack of Smad3 prevents renal fibrosis, monocyte influx, and TGF-β1 upregulation. (a and b) Immunofluorescence of type I collagen in obstructed kidneys of WT (a) and Smad3-null (KO) (b) mice at day 14 after UUO. (c) Hydroxyproline content in obstructed kidneys from WT and KO mice and sham-operated WT mice (Sham). (d and e) Immunofluorescence of F4/80 antigen, a mouse monocyte marker, in obstructed kidneys from WT (d) and KO (e) mice at day 14 after UUO. DAPI (blue) was used for nuclear staining. Scale bars: 20 μm. (f) Number of monocytes per unit area in obstructed kidneys from WT and KO mice with UUO and sham-operated WT mice (Sham). (g) Northern blot of TGF-β1 mRNA in kidneys from WT and KO mice with UUO and sham-operated counterparts (Sham). (h) Active and total TGF-β1 concentrations as determined by immunoassay in kidneys of WT and KO mice and sham-operated mice (Sham). Results are means ± standard deviation of four to five samples. *P < 0.01 compared with Sham or KO.