Renal liver-type fatty acid binding protein attenuates angiotensin II-induced renal injury.

To investigate the role of human liver-type fatty acid binding protein (hL-FABP) in angiotensin (Ang) II-induced renal injury, Ang II was infused systemically into hL-FABP chromosomal transgenic (Tg) and wild-type (WT) mice (Tg-Ang II and WT-Ang II) for 28 days. Control mice were injected with saline only (Tg-control and WT-control). hL-FABP was expressed in proximal tubules of Tg mice. After a high-dose injection of Ang II, renal gene and protein expressions of hL-FABP in Tg-Ang II mice increased significantly compared with Tg-control mice. Urinary excretion of L-FABP was significantly greater in Tg-Ang II than in Tg-control mice. Blood pressure levels in both groups increased to a similar extent. Upregulation of monocyte chemoattractant protein 1 expression, macrophage infiltration in the interstitium, tubulointerstitial damage, and depositions of type I and III collagens were observed in both Tg-Ang II and WT-Ang II mice. However, these effects were less pronounced in Tg-Ang II compared with WT-Ang II mice. The level of renal N-(hexanoyl)lysine, an oxidative stress marker, was significantly higher in WT-Ang II than in Tg-Ang II mice. In conclusion, renal hL-FABP reduced oxidative stress in Ang II-induced renal injury and attenuated tubulointerstitial damage.