Mice deficient in α-actinin-4 have severe glomerular disease
J. Clin. Invest. Claudine H. Kos, et al. 111:1683 doi:10.1172/JCI17988 [Go to this article.]

Figure 3
(a and b) Kidney sections from 4-week-old mice, stained with H&E. Actn4^+/+ kidney (a) and Actn4^–/– kidney (b) photographed at ×10 magnification. (c and d) At higher magnification (×40), glomerular abnormalities are clearly visible in the Actn4^–/– mouse (d), but not in the Actn4^+/+ littermate (c): the Actn4^–/– kidney shows FSGS, with protein in tubules and areas of glomerular capillary collapse. A diseased glomerulus is indicated by an arrow (labeled “G”). A tubule filled with proteinaceous material is also indicated by an arrow (labeled “T”). (e and f) Kidney sections from 10-week-old mice, stained with H&E. (e) Actn4^+/+ kidney; (f) Actn4^–/– kidney. The Actn4^–/– kidney shows extensive disease, with sclerosed glomeruli, dilated tubules with proteinaceous material, and disrupted architecture. (g) Gross appearance of Actn4^+/+ (left) and Actn4^–/– (right) kidneys from 10-week-old mice.