Lipid peroxidation in human proteinuric disease

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Lipid peroxidation in human proteinuric disease Marja-Liisa Solin, Heikki Ahola, Anni Haltia, Fulvio Ursini, Tom Montine, Antonella Roveri, Dontscho Kerjaschki, Harry Holthöfer  Kidney International  Volume 59, Issue 2, Pages 481-487 (February 2001) DOI: 10.1046/j.1523-1755.2001.059002481.x Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 1 Immunostaining of congenital nephrotic syndrome of the Finnish type (CNF) patient kidneys (A and B) and normal human kidney cortex (C) with anti–4-hydroxynonenal (anti-4-HNE) antibodies. Strong, patchy reactivity at areas facing the urinary space in glomeruli is obvious in CNF kidneys (A and B, arrows), whereas faint background reactivity is seen in normal kidney (C). Bar 10 μm (A and C) and 3 μm (B). Kidney International 2001 59, 481-487DOI: (10.1046/j.1523-1755.2001.059002481.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 2 Immunostaining of CNF patient kidneys (a and b), biopsy sample of membranous glomerulonephritis (c), diabetic nephropathy (d), and normal human kidney (e) with anti-MDA antibodies. Reactivity is seen in apparent podocytes (arrows in a and b) but also in the mesangium and at the basement membranes (b–d). (Bar = 10 μm for a, c, and e; and 3 μm for b and d). Kidney International 2001 59, 481-487DOI: (10.1046/j.1523-1755.2001.059002481.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 3 Reactivity of anti-phospholipid hydroperoxide glutathione peroxidase (anti-PHGPx) antibodies in normal kidney cortex (a) and in CNF kidney (b). Note the prominent reactivity in a podocyte-like pattern in (a, arrows) with a decreased reactivity pattern in CNF (b). Magnification ×260. Kidney International 2001 59, 481-487DOI: (10.1046/j.1523-1755.2001.059002481.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 4 RNA expression levels of kidney cortical cytochrome-c-oxidase (COX) subunits encoded by the mitochondrial (COX I, COX II) and nuclear genome (COX IV, COX VIb) in control human kidney (NHK;) and CNF (). When the values of the control kidneys are normalized to 1.0, the values of the mitochondrially encoded components are decreased to 25.9 and 27.3% of the control (P < 0.001 for both COX I and COX II vs. controls), whereas no significant change in the nuclearly encoded components is seen. Kidney International 2001 59, 481-487DOI: (10.1046/j.1523-1755.2001.059002481.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 5 Semiquantitative RT-PCR of CNF and normal human kidney glomeruli (NHG 1 and NHG 2) with transcripts of mitochondrially encoded cytochromes I (COX I) and cytochrome b (CYT b), nuclearly encoded cytochrome 7A (COX 7A) and phospholipid hydroperoxide glutathione peroxidase (PHGPx). cDNAs were serially diluted to the range of linear amplification (10-1 to 10-4); β-actin expression was used to obtain comparable cDNA concentrations in all samples. Note the down-regulation of COX I, CYT b, and PHGPx. Kidney International 2001 59, 481-487DOI: (10.1046/j.1523-1755.2001.059002481.x) Copyright © 2001 International Society of Nephrology Terms and Conditions