Lipoproteins accumulate in immune deposits and are modified by lipid peroxidation in passive Heymann nephritis.
Proteinuria in passive Heymann nephritis is primarily caused by reactive oxygen species that are produced by glomerular cells. Reactive oxygen species apparently exert their damaging effects on the glomerular filter by lipid peroxidation and subsequent adduct formation on matrix proteins of glomerular basement membranes. This raised the question as to the source of polyunsaturated fatty acids required as substrates for lipid peroxidation. Here we have localized by immunocytochemistry rat apolipoprotein E and apolipoprotein B within subepithelial immune deposits. Moreover, apolipoprotein B extracted from isolated glomeruli of proteinuric passive Heymann nephritis rats shows degradation and lipid peroxidation adduct formation, similar to apoproteins of oxidized lipoproteins in atherosclerotic lesions. These data provide evidence that lipoproteins accumulate within immune deposits and suggest that their lipids generate lipid-peroxidation-derived reactive compounds.
Exner
M
M
Division of Ultrastructural Pathology and Cell Biology, University of Vienna, Austria.
Susani
M
M
Witztum
J L
JL
Hovorka
A
A
Curtiss
L K
LK
Spitzauer
S
S
Kerjaschki
D
D
D000818:Animals; D001055:Apolipoproteins B / Q000378:metabolism*; D001057:Apolipoproteins E / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000097:blood / Q000378:metabolism* / Q000652:urine; D007678:Kidney Glomerulus / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D011507:Proteinuria; D051381:Rats; D017207:Rats, Sprague-Dawley
D001055:Apolipoproteins B; D001057:Apolipoproteins E; D002784:Cholesterol