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. 2011 Oct;22(10):1821–1833. doi: 10.1681/ASN.2011010038

Figure 2.

Figure 2.

csCSF-1 or spCSF-1, but not sgCSF-1, restored kidney disease in CSF-1-deficient MRL-Faslpr mice. (A) We analyzed tubular and glomerular pathology in TgC/+, TgCS/+, TgSPP/+, and TgSGP/+ mice with advancing disease (1.5, 3.0, and 5.0 months of age); WT and Csf1op/op mice served as controls. The data are the means ± SEM, n = 6 to 8/group. (B) Loss of renal function (albuminuria and blood urea nitrogen [BUN]) is accelerated in WT mice in comparison with TgCS/+ and TgSPP/+ mice. In contrast, TgSGP/+ and Csf1op/op mice remain protected from loss of renal function. Serum control BUN for MRL-++ and B6 mice are denoted by a dotted line. The values are the means ± SEM, n = 8 to 14/group.