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. Author manuscript; available in PMC: 2013 Dec 17.
Published in final edited form as: Arthritis Rheum. 2010 May;62(5):10.1002/art.27382. doi: 10.1002/art.27382

Figure 5.

Figure 5

Focal interstitial glomerulosclerosis in Col1a2-CTGF–transgenic mouse kidneys. A–J, Kidney tissue specimens from WT littermate controls (A, C, E, G, and I) compared with those from adult Col1a2-CTGF–transgenic mice (B, D, F, H, and J). Masson's trichrome staining was increased in the basement membrane surrounding the glomeruli of Col1a2-CTGF–transgenic mouse kidneys (A and B). Immunostaining with type IV collagen antibody demonstrated that the accumulated collagen in the interstitium of Col1a2-CTGF–transgenic mice consisted of type IV collagen (C and D). Immunostaining with CTGF antibody showed increased CTGF expression in the glomeruli, surrounding interstitium, in Col1a2-CTGF–transgenic compared with WT mice (E and F). Small blood vessels in the kidney sections stained with Masson's trichrome showed increased collagen deposition around the blood vessels and in the intima in Col1a2-CTGF–transgenic mice compared with WT littermates (G and H). Immunostaining with CD31, a marker for endothelial cells, revealed increased proliferation of endothelial cells in small blood vessels of Col1a2-CTGF–transgenic mice and normal distribution of endothelial cells in WT mice (I and J). K and L, Differential interference contrast overlays of I and J, respectively. See Figure 1 for definitions.