Key result
Expression of human liver-type fatty acid-binding protein ameliorated tubulointerstitial damage in aldosterone-induced renal injury via reducing oxidative stress and suppressing the intrarenal RAS.
Expression of hL-FABP protects against aldosterone-induced tubulointerstitial renal injury by reducing oxidative stress and suppressing the intrarenal renin-angiotensin system.
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Hypothesis-generating for hL-FABP as renoprotective target in aldosterone excess; human trials needed before clinical consideration.
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.
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Ichikawa et al. (2014) studied Aldosterone-induced renal injury. hL-FABP chromosomal transgenic expression vs. Wild-type (WT) mice was evaluated on Tubulointerstitial damage and oxidative stress. Expression of human liver-type fatty acid-binding protein ameliorated tubulointerstitial damage in aldosterone-induced renal injury via reducing oxidative stress and suppressing the intrarenal RAS.
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