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. 1999 Feb 1;103(3):331–340. doi: 10.1172/JCI3858

Figure 6.

Figure 6

Pathological changes in 4.1R–/– tissues. Hematoxylin- and eosin-stained sections of (a) normal and (b) 4.1R–/– spleen sections. Note the effacement of the splenic nodules by the dramatic expansion of the red pulp areas in 4.1R–/– spleen. Prussian blue–stained (c) normal and (d) 4.1R–/– spleen. Iron deposition is decreased in 4.1R–/– spleen red pulp areas due to increased use by rapidly proliferating erythroid precursors. Prussian blue–stained (e) normal and (f) 4.1R–/– liver. Hematopoietic foci (arrows) are frequent and liver iron deposition increased in 4.1R–/– mice, reflecting increased destruction of 4.1-null red cells. Note that no iron deposition is seen in areas of proliferating erythroid precursors, i.e., liver hematopoietic foci (arrows). Prussian blue stains of (g) normal and (h) 4.1R–/– kidney. Note the extensive deposition of iron in 4.1R–/– proximal tubules (arrows) and Bowman's capsule (arrowhead), indicating severe intravascular hemolysis of 4.1R-null red cells. Bar, 100 μM.