TY - JOUR
T1 - Virus-mediated transduction of apolipoprotein E (ApoE)-Sendai develops lipoprotein glomerulopathy in ApoE-deficient mice
AU - Ishigaki, Yasushi
AU - Oikawa, Shinichi
AU - Suzuki, Takashi
AU - Usui, Shinichi
AU - Magoori, Kenta
AU - Kim, Dong Ho
AU - Suzuki, Hiroyuki
AU - Sasaki, Jun
AU - Sasano, Hironobu
AU - Okazaki, Mitsuyo
AU - Toyota, Takayoshi
AU - Saito, Takao
AU - Yamamoto, Tokuo T.
PY - 2000/10/6
Y1 - 2000/10/6
N2 - Lipoprotein glomerulopathy (LPG) is a unique renal disease characterized by thrombus-like substances in markedly dilated glomerular capillaries, dysbetalipoproteinemia, and elevated plasma concentrations of apoE. Recent studies identified several apoE mutations in patients with LPG, including apoE2(R145P) Sendal (apoE-Sendai). Virus-mediated transduction of apoE-Sendai in apoE-deficient hypereholesterolemic mice resulted in insufficient correction of hypercholesterolemia and a marked and temporal induction of plasma triglyceride levels. In vitro binding studies showed that apoE-Sendal has a reduced affinity for the low density lipoprotein receptor, suggesting that dysbetalipoproteinemia in LPG is caused by the apoE mutation. Furthermore, histological examination revealed marked intraglomerular depositions of apoE-containing lipoproteins in mice injected with apoE-Sendai virus. These LPG-like depositions were detected 6 days after virus injection and were sustained for at least 69 days. Our results demonstrated that apoE-Sendai is an etiological cause of LPG.
AB - Lipoprotein glomerulopathy (LPG) is a unique renal disease characterized by thrombus-like substances in markedly dilated glomerular capillaries, dysbetalipoproteinemia, and elevated plasma concentrations of apoE. Recent studies identified several apoE mutations in patients with LPG, including apoE2(R145P) Sendal (apoE-Sendai). Virus-mediated transduction of apoE-Sendai in apoE-deficient hypereholesterolemic mice resulted in insufficient correction of hypercholesterolemia and a marked and temporal induction of plasma triglyceride levels. In vitro binding studies showed that apoE-Sendal has a reduced affinity for the low density lipoprotein receptor, suggesting that dysbetalipoproteinemia in LPG is caused by the apoE mutation. Furthermore, histological examination revealed marked intraglomerular depositions of apoE-containing lipoproteins in mice injected with apoE-Sendai virus. These LPG-like depositions were detected 6 days after virus injection and were sustained for at least 69 days. Our results demonstrated that apoE-Sendai is an etiological cause of LPG.
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U2 - 10.1074/jbc.M005906200
DO - 10.1074/jbc.M005906200
M3 - Article
C2 - 10903326
AN - SCOPUS:0034613278
VL - 275
SP - 31269
EP - 31273
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 40
ER -