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Nephrotic syndrome causes upregulation of HDL endocytic receptor and PDZK-1-dependent downregulation of HDL docking receptor

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Author(s)
Nosratola D. VaziriPavan GollapudiSeungyeup HanGuity FarahmandJun YuanArdeshir RahimiHamid Moradi
Keimyung Author(s)
Han, Seung Yeup
Department
Dept. of Internal Medicine (내과학)
Journal Title
Nephrol Dial Transplant
Issued Date
2011
Volume
26
Issue
10
Keyword
atherosclerosiscardiovascular diseasedyslipidemiaproteinuriareverse cholesterol transport
Abstract
Background. Nephrotic syndrome (NS) is associated with
dysregulation of lipid/lipoprotein metabolism and impaired
high-density lipoprotein (HDL)-mediated reverse cholesterol
transport and atherosclerosis.HDLserves as vehicle for transport
of surplus lipids from the peripheral tissues for disposal
in the liver via two receptors: (i) scavenger receptor class B
type I (SR-BI) which serves as a docking receptor, enabling
HDL to unload its lipid cargo and return to circulation to
repeat the cycle, and (ii) beta chain ATP synthase which
serves as the endocytic receptor mediating removal and
catabolism of lipid-poorHDL. SR-BI abundance is regulated
by PDZ-containing kidney protein 1 (PDZK1), a multifunctional
protein, which prevents SRB-1 degradation at the
post-translational level. This study explored the effect of
NS on hepatic expression of these important molecules.
Methods. Gene expression, protein abundance and immunohistological
appearance of the above proteins were measured
in the liver of rats with puromycin-induced NS and
control rats.
Results. The nephrotic animals exhibited severe proteinuria,
hypoalbuminemia, hypercholesterolemia, hypertriglyceridemia,
reduced HDL/total cholesterol ratio, normal
glomerular filtration rate, significant upregulation of the
endocytic HDL receptor messenger RNA (mRNA) and
protein (P < 0.005) and significant reduction of SR-BI
protein (P < 0.002) despite its normal mRNA abundance.
The reduction in SR-BI protein abundance in NS animals
was accompanied by parallel reductions in PDZK1 mRNA
(P ¼ 0.02) and protein abundance (P ¼ 0.012).
Conclusions. NS results in elevation of hepatic HDL endocytic
receptor and deficiency of HDL docking receptor. The
latter is associated with and, in part, mediated by downregulation
of PDZK1. Together, these abnormalities can increase
catabolism and diminish recycling of HDL and contribute to
the defective reverse cholesterol/lipid transport in NS.
Keywords: atherosclerosis; cardiovascular disease; dyslipidemia;
proteinuria; reverse cholesterol transport
Keimyung Author(s)(Kor)
한승엽
Publisher
School of Medicine
Citation
Nosratola D. Vaziri et al. (2011). Nephrotic syndrome causes upregulation of HDL endocytic receptor and PDZK-1-dependent downregulation of HDL docking receptor. Nephrol Dial Transplant, 26(10), 3118–3123. doi: 10.1093/ndt/gfr136
Type
Article
ISSN
0931-0509
Source
https://academic.oup.com/ndt/article/26/10/3118/1905384
DOI
10.1093/ndt/gfr136
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/33483
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Internal Medicine (내과학)
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