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. 2010 Jul;21(7):1145–1156. doi: 10.1681/ASN.2009090991

Figure 3.

Figure 3.

Deletion of FAK in podocytes diminishes podocyte injury and proteinuria. (A) ACR from FAKfl/fl;Pod-Cre and FAK+/+;Pod-Cre mice after LPS at indicated time points. ACR measured from samples at 0, 12, 24, 36, and 72 hours (n = 8). *P < 0.001 at 12 hours; **P < 0.001 at 24 hours; ***P < 0.001 at 36 hours. (B) Representative Western blot from isolated primary podocyte cell lysates from FAKfl/fl;Pod-Cre and FAK+/+;Pod-Cre mice stimulated with or without LPS and immunoblotted with α-FAK, α-pFAK 397, and α-α-tubulin. (C) Representative electron microscopy image of FAKfl/fl; Pod-Cre and FAK+/+;Pod-Cre mouse podocytes stimulated with or without LPS. (D) Quantification of C (n = 3). ∧P < 0.01. (E) Representative hematoxylin and eosin staining of glomeruli from FAK+/+;Pod-Cre and FAKfl/fl;Pod-Cre mouse after rabbit anti-mouse GBM treatment at the indicated time points. (F) Quantification of glomerular crescent formation (expressed as percentage of 25 glomeruli examined per mouse) (n = 5, #P < 0.005). (G) ACR at day 6 after injection of α-rabbit-anti-mouse GBM in FAKfl/fl;Pod-Cre and FAK+/+;Pod-Cre mice (n = 7). ∧P < 0.01. (H) Serum creatinine at day 6 after injection of α-rabbit-anti-mouse GBM in FAKfl/fl;Pod-Cre and FAK+/+;Pod-Cre mice (n = 7). &P < 0.05.