Lectin-like oxidized LDL receptor-1 (LOX-1) expression in the tubulointerstitial area likely plays an important role in human diabetic nephropathy

Intern Med. 2009;48(4):189-94. doi: 10.2169/internalmedicine.48.1251. Epub 2009 Feb 16.

Abstract

Objective: Diabetic nephropathy (DN) is a common cause of end-stage renal disease. However, the precise mechanism of DN, which involves the role of lipid, is still not fully understood. Lectin-like oxidized LDL receptor-1 (LOX-1) is a type II single-transmembrane protein that binds oxidized low density lipoprotein (Ox-LDL). This study examined the expression of LOX-1 mRNA in renal tissues from type 2 diabetes patients with DN using in situ hybridization (ISH).

Patients and methods: Renal tissues were obtained from 15 type 2 patients with DN and 5 minimal change nephrotic syndrome (MCNS), membranous nephropathy (MN) and normal human kidney (NHK). Glomerular and tubulointerstitial LOX-1 mRNA expression was evaluated by ISH. Results The cells positive for LOX-1 mRNA were identified in the glomeruli of DN, MCNS, MN and NHK, however, there was no positive signal in the tubulointerstitial area in MCNS and NHK. Some cells positive for LOX-1 mRNA were detectable in the tubulointerstitial area in DN and MN. In the results of glomerular staining, there was no significant difference between them. There was a significant correlation between the tubulointerstitial LOX-1 expression and the degree of the tubulointerstitial damage and urinary protein in DN.

Conclusion: Increased expression of LOX-1 mRNA in the tubulointerstitial area may be closely linked to the development and progression of human DN, and in particular the tubulointerstitial damage.

MeSH terms

  • Adult
  • Case-Control Studies
  • Diabetic Nephropathies / metabolism*
  • Female
  • Humans
  • In Situ Hybridization
  • Kidney / metabolism*
  • Male
  • Middle Aged
  • Nephrosis, Lipoid / metabolism
  • RNA, Messenger / metabolism
  • Scavenger Receptors, Class E / metabolism*

Substances

  • RNA, Messenger
  • Scavenger Receptors, Class E