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. 2016 Jan 7;27(8):2257–2264. doi: 10.1681/ASN.2015060683

Figure 1.

Figure 1.

Stimulation of AT1A receptors on T lymphocytes attenuates cisplatin-induced AKI. (A and B) Representative images of kidney sections from CD4-Cre+ mT/mG mice at 12, 24, or 72 hours after (A) saline or (B) cisplatin injection. (C–M) Renal function and injury parameters in WT (TWT) mice and CD4-Cre+ Agtr1afl/fl (TKO) mice at 72 hours after saline or cisplatin treatment. (C) BUN and (D) sCr (n=6 for saline and n≥10 for cisplatin). (E–H) Representative images of kidney sections from saline– and cisplatin–treated (E and G) TWT and (F and H) TKO mice, respectively. *Tubular dilation (mild injury); #lysed tubules (severe injury with cell death); →, loss of brush border (mild injury). (I) Semiquantitative scoring of renal pathology. (J and K) Renal mRNA expression of (J) NGAL and (K) TNF-α. (L) Serum and (M) whole–kidney TNF-α protein content. GAPDH, glyceraldehyde-3-phosphate dehydrogenase.