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Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration.

Publication ,  Journal Article
Ishizaka, N; Aizawa, T; Yamazaki, I; Usui, S-I; Mori, I; Kurokawa, K; Tang, S-S; Ingelfinger, JR; Ohno, M; Nagai, R
Published in: Lab Invest
January 2002

Acute experimental iron loading causes iron to accumulate in the renal tissue. The accumulation of iron may play a role in enhancing oxidant-induced tubular injury by producing increased amounts of reactive oxygen species. From findings in cells from heme oxygenase-1 (HO-1)-deficient mice, HO-1 is postulated to prevent abnormal intracellular iron accumulation. Recently, it has been reported that HO-1 is induced in the renal tubular epithelial cells, in which iron is deposited after iron loading, and that this HO-1 induction may be involved in ameliorating iron-induced renal toxicity. We previously showed that chronic administration of angiotensin II to rats induces HO-1 expression in the tubular epithelial cells. These observations led us to investigate whether there is a link between iron deposition and HO-1 induction in renal tubular cells in rats undergoing angiotensin II infusion. In the present study, rats were given angiotensin II for continuously 7 days. Prussian blue staining revealed the distinct deposits of iron in the proximal tubular epithelial cells after angiotensin II administration. Electron microscopy demonstrated that iron particles were present in the lysosomes of these cells. Histologic and immunohistochemical analyses showed that stainable iron and immunoreactive ferritin and HO-1 were colocalized in the tubular epithelial cells. Treatment of angiotensin II-infused rats with an iron chelator, deferoxamine, blocked the abnormal iron deposition in kidneys and also the induced expression of HO-1 and ferritin expression. Furthermore, deferoxamine treatment suppressed the angiotensin II-induced increase in the urinary excretion of protein and N-acetyl-beta-D-glucosaminidase, a marker of tubular injury; however, deferoxamine did not affect the angiotensin II-induced decrease in glomerular filtration rate. These results suggest that angiotensin II causes renal injury, in part, by inducing the deposition of iron in the kidney.

Duke Scholars

Published In

Lab Invest

DOI

ISSN

0023-6837

Publication Date

January 2002

Volume

82

Issue

1

Start / End Page

87 / 96

Location

United States

Related Subject Headings

  • Urothelium
  • Rats
  • Proteinuria
  • Pathology
  • Mice, Knockout
  • Mice
  • Membrane Proteins
  • Kidney Tubules
  • Kidney Medulla
  • Kidney Cortex
 

Citation

APA
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ICMJE
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Ishizaka, N., Aizawa, T., Yamazaki, I., Usui, S.-I., Mori, I., Kurokawa, K., … Nagai, R. (2002). Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration. Lab Invest, 82(1), 87–96. https://doi.org/10.1038/labinvest.3780398
Ishizaka, Nobukazu, Toru Aizawa, Ieharu Yamazaki, Shin-ichi Usui, Ichiro Mori, Kiyoshi Kurokawa, Shiow-Shih Tang, Julie R. Ingelfinger, Minoru Ohno, and Ryozo Nagai. “Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration.Lab Invest 82, no. 1 (January 2002): 87–96. https://doi.org/10.1038/labinvest.3780398.
Ishizaka N, Aizawa T, Yamazaki I, Usui S-I, Mori I, Kurokawa K, et al. Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration. Lab Invest. 2002 Jan;82(1):87–96.
Ishizaka, Nobukazu, et al. “Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration.Lab Invest, vol. 82, no. 1, Jan. 2002, pp. 87–96. Pubmed, doi:10.1038/labinvest.3780398.
Ishizaka N, Aizawa T, Yamazaki I, Usui S-I, Mori I, Kurokawa K, Tang S-S, Ingelfinger JR, Ohno M, Nagai R. Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration. Lab Invest. 2002 Jan;82(1):87–96.

Published In

Lab Invest

DOI

ISSN

0023-6837

Publication Date

January 2002

Volume

82

Issue

1

Start / End Page

87 / 96

Location

United States

Related Subject Headings

  • Urothelium
  • Rats
  • Proteinuria
  • Pathology
  • Mice, Knockout
  • Mice
  • Membrane Proteins
  • Kidney Tubules
  • Kidney Medulla
  • Kidney Cortex