|  Help  |  About  |  Contact Us

Publication : Human liver-type fatty acid-binding protein protects against tubulointerstitial injury in aldosterone-induced renal injury.

First Author  Ichikawa D Year  2015
Journal  Am J Physiol Renal Physiol Volume  308
Issue  2 Pages  F114-21
PubMed ID  25339700 Mgi Jnum  J:237452
Mgi Id  MGI:5812762 Doi  10.1152/ajprenal.00469.2014
Citation  Ichikawa D, et al. (2015) Human liver-type fatty acid-binding protein protects against tubulointerstitial injury in aldosterone-induced renal injury. Am J Physiol Renal Physiol 308(2):F114-21
abstractText  To demonstrate the renoprotective function of human liver-type fatty acid-binding protein (hL-FABP) expressed in proximal tubules in aldosterone (Aldo)-induced renal injury, hL-FABP chromosomal transgenic (Tg) and wild-type (WT) mice received systemic Aldo infusions (Tg-Aldo and WT-Aldo, respectively) were given 1% NaCl water for 28 days. In this model, elevation of systolic blood pressure, monocyte chemoattractant protein-1 expression, macrophage infiltration in the interstitium, tubulointerstitial damage, and depositions of type I and III collagens were observed. Elevation of systolic blood pressure did not differ in WT-Aldo vs. Tg-Aldo animals, however, renal injury was suppressed in Tg-Aldo compared with WT-Aldo mice. Dihydroethidium fluorescence was used to evaluate reactive oxidative stress, which was suppressed in Tg-Aldo compared with WT-Aldo mice. Gene expression of angiotensinogen in the kidney was upregulated, and excretion of urinary angiotensinogen was increased in WT-Aldo mice. This exacerbation was suppressed in Tg-Aldo mice. Expression of hL-FABP was upregulated in proximal tubules of Tg-Aldo mice. Urinary excretion of hL-FABP was significantly greater in Tg-Aldo than in Tg-control mice. In conclusion, hL-FABP ameliorated the tubulointerstitial damage in Aldo-induced renal injury via reducing oxidative stress and suppressing activation of the intrarenal renin-angiotensin system.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

1 Bio Entities

Trail: Publication

0 Expression