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Am J Physiol Renal Physiol. 2015 Jan 15;308(2):F114-21. doi: 10.1152/ajprenal.00469.2014. Epub 2014 Oct 22.

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

Author information

1
Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan; and.
2
Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan; and Department of Anatomy, St. Marianna University School of Medicine, Kanagawa, Japan a2kamijo@marianna-u.ac.jp.
3
Department of Anatomy, St. Marianna University School of Medicine, Kanagawa, Japan.
4
Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kanagawa, Japan; and Department of Anatomy, St. Marianna University School of Medicine, Kanagawa, Japan.

Abstract

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.

KEYWORDS:

L-FABP; activation of the intrarenal renin-angiotensin system; aldosterone; oxidative stress; tubulointerstitial damage

PMID:
25339700
DOI:
10.1152/ajprenal.00469.2014
[Indexed for MEDLINE]
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