Liver-type fatty acid-binding protein attenuates renal injury induced by unilateral ureteral obstruction

Am J Pathol. 2006 Oct;169(4):1107-17. doi: 10.2353/ajpath.2006.060131.

Abstract

Liver-type fatty-acid-binding protein (L-FABP), which has high affinity for long-chain fatty acid oxidation products, may be an effective endogenous antioxidant. To examine the role of L-FABP in tubulointerstitial damage, we used a unilateral ureteral obstruction (UUO) model. We established human L-FABP (hL-FABP) gene transgenic (Tg) mice and compared the tubulointerstitial pathology of the Tg mice (n = 23) with that of the wild-type (WT) mice (n = 23). Mice were sacrificed on days 2, 4, 5, or 7 after UUO. Although mouse L-FABP was not expressed in WT mice, hL-FABP was expressed in the proximal tubules of the Tg mice with UUO (UUO-Tg) and in sham-operated Tg mice. The expression of renal hL-FABP was significantly increased in UUO-Tg compared with sham-operated Tg mice. The number of macrophages (F4/80) infiltrating the interstitium and the level of expression of MCP-1 and MCP-3 were significantly lower in UUO-Tg kidneys compared with UUO-WT kidneys. In UUO-Tg kidneys, the degree of the tubulointerstitial injury and the deposition of type I collagen were significantly lower than that of UUO-WT kidneys. On day 7, lipid peroxidation product accumulated in the UUO-WT kidneys but not in that of UUO-Tg kidneys. In conclusion, renal L-FABP may reduce the oxidative stress in the UUO model, ameliorating tubulointerstitial damage.

MeSH terms

  • Animals
  • Carboxypeptidases A / metabolism
  • Chemokine CCL2 / metabolism
  • Collagen Type I / analysis
  • Collagen Type I / metabolism
  • Fatty Acid-Binding Proteins / analysis
  • Fatty Acid-Binding Proteins / genetics
  • Fatty Acid-Binding Proteins / metabolism*
  • Kidney Diseases / metabolism*
  • Kidney Diseases / pathology
  • Kidney Tubules / chemistry
  • Kidney Tubules / metabolism*
  • Kidney Tubules / pathology
  • Lipids / blood
  • Mice
  • Mice, Transgenic
  • Oxidative Stress
  • Transforming Growth Factor alpha / metabolism
  • Ureteral Obstruction / pathology

Substances

  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Collagen Type I
  • FABP1 protein, human
  • Fatty Acid-Binding Proteins
  • Lipids
  • Transforming Growth Factor alpha
  • Carboxypeptidases A
  • Cpa3 protein, mouse