Figure 5
Figure 5. Low TF expression prevents glomerular injury in mouse aPL antibody (FB1 and FC1)– and human aPL antibody (aPL-IgG)–treated mice. (A) BUN levels. Mice expressing low levels of TF were protected from BUN increase induced by FB1, FC1, and aPL-IgG antibodies. *Different from wild-type (P < .005). (B) Genetic diminution of TF prevented ACR increase in FB1-, FC1-, and aPL-IgG–treated mice. *Different from wild-type (P < .01). (C) Transmission electron micrograph of a glomerulus from low TF mice treated with FB1 (i), FC1 (ii), and aPL-IgG (iii). Low expression of TF prevented glomerular injury in these mice. Well-preserved endothelial cells with abundant fenestrations were observed (—). Six or 7 mice were studied in each experimental group. (D) Glomerular injury scores. FB1-, FC1-, and aPL-IgG–treated mice showed glomerular injury scores significantly lower than wild-type mice. *Different from wild-type mice (P < .005).

Low TF expression prevents glomerular injury in mouse aPL antibody (FB1 and FC1)– and human aPL antibody (aPL-IgG)–treated mice. (A) BUN levels. Mice expressing low levels of TF were protected from BUN increase induced by FB1, FC1, and aPL-IgG antibodies. *Different from wild-type (P < .005). (B) Genetic diminution of TF prevented ACR increase in FB1-, FC1-, and aPL-IgG–treated mice. *Different from wild-type (P < .01). (C) Transmission electron micrograph of a glomerulus from low TF mice treated with FB1 (i), FC1 (ii), and aPL-IgG (iii). Low expression of TF prevented glomerular injury in these mice. Well-preserved endothelial cells with abundant fenestrations were observed (—). Six or 7 mice were studied in each experimental group. (D) Glomerular injury scores. FB1-, FC1-, and aPL-IgG–treated mice showed glomerular injury scores significantly lower than wild-type mice. *Different from wild-type mice (P < .005).

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