Soluble LR11 competes with amyloid β in binding to cerebrospinal fluid-high-density lipoprotein.


Journal

Clinica chimica acta; international journal of clinical chemistry
ISSN: 1873-3492
Titre abrégé: Clin Chim Acta
Pays: Netherlands
ID NLM: 1302422

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 22 04 2018
revised: 06 11 2018
accepted: 14 11 2018
pubmed: 19 11 2018
medline: 19 3 2019
entrez: 19 11 2018
Statut: ppublish

Résumé

LR11 is a member of the low-density lipoprotein (LDL) receptor family with high expression in neurons. Some cell surface LR11 is cleaved and secreted into the cerebrospinal fluid (CSF) as soluble LR11 (sLR11). Patients with Alzheimer's disease (AD), particularly apolipoprotein E4 carriers, have high CSF-sLR11 and low CSF-amyloid β (Aβ) concentrations. Therefore, we assessed whether sLR11 is bound to CSF-high-density lipoprotein (HDL) and whether sLR11 competes with Aβ in binding to apoE in CSF-HDL. We measured CSF-sLR11 concentrations (50 controls and 16 patients with AD) using enzyme immunoassay. sLR11 and apoE distribution in the CSF was evaluated using non-denaturing two-dimensional gel electrophoresis (N-2DGE). ApoE bound to sLR11 or Aβ was identified using co-immunoprecipitation assay. CSF-sLR11 concentrations were higher in patients with AD than controls (adjusted for sLR11 using phospholipid). N-2DGE analysis showed that sLR11 and Aβ comigrated with a large apoE-containing CSF-HDL. Moreover, fewer apoE was bound to Aβ when a higher amount of apoE was bound to sLR11 in patients with AD who presented with ε4/4. sLR11 binds to CSF-HDL and competes with Aβ in binding to apoE in CSF-HDL, indicating that sLR11 affects Aβ clearance via CSF-HDL.

Sections du résumé

BACKGROUND BACKGROUND
LR11 is a member of the low-density lipoprotein (LDL) receptor family with high expression in neurons. Some cell surface LR11 is cleaved and secreted into the cerebrospinal fluid (CSF) as soluble LR11 (sLR11). Patients with Alzheimer's disease (AD), particularly apolipoprotein E4 carriers, have high CSF-sLR11 and low CSF-amyloid β (Aβ) concentrations. Therefore, we assessed whether sLR11 is bound to CSF-high-density lipoprotein (HDL) and whether sLR11 competes with Aβ in binding to apoE in CSF-HDL.
METHODS METHODS
We measured CSF-sLR11 concentrations (50 controls and 16 patients with AD) using enzyme immunoassay. sLR11 and apoE distribution in the CSF was evaluated using non-denaturing two-dimensional gel electrophoresis (N-2DGE). ApoE bound to sLR11 or Aβ was identified using co-immunoprecipitation assay.
RESULTS RESULTS
CSF-sLR11 concentrations were higher in patients with AD than controls (adjusted for sLR11 using phospholipid). N-2DGE analysis showed that sLR11 and Aβ comigrated with a large apoE-containing CSF-HDL. Moreover, fewer apoE was bound to Aβ when a higher amount of apoE was bound to sLR11 in patients with AD who presented with ε4/4.
CONCLUSION CONCLUSIONS
sLR11 binds to CSF-HDL and competes with Aβ in binding to apoE in CSF-HDL, indicating that sLR11 affects Aβ clearance via CSF-HDL.

Identifiants

pubmed: 30448281
pii: S0009-8981(18)30605-3
doi: 10.1016/j.cca.2018.11.024
pii:
doi:

Substances chimiques

Amyloid beta-Peptides 0
Apolipoproteins E 0
LDL-Receptor Related Proteins 0
Lipoproteins 0
Membrane Transport Proteins 0
SORL1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

29-34

Informations de copyright

Copyright © 2018 Elsevier B.V. All rights reserved.

Auteurs

Kouji Yano (K)

Center for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan; Department of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan.

Satoshi Hirayama (S)

Department of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan; Department of Clinical Laboratory Medicine, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan. Electronic address: sthiraya@juntendo.ac.jp.

Naomi Misawa (N)

Department of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan.

Ayaka Furuta (A)

Department of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan.

Tsuyoshi Ueno (T)

Department of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan.

Yumiko Motoi (Y)

Department of Diagnosis, Prevention and Treatment of Dementia, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan; Department of Neurology, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan.

Utako Seino (U)

Bioscience Medical Research Center, Niigata University Medical & Dental Hospital, Asahimachi-Tohri 1-754, Chuo-ku, Niigata, Niigata 951-8510, Japan.

Hiroyuki Ebinuma (H)

Sekisui Medical Tsukuba Research Institute, Yoshiwara 3262-12, Ami-machi, Inashiki-gun, Ibaraki 301-1155, Japan.

Takeshi Ikeuchi (T)

Department of Molecular Genetics, Brain Research Institute, Niigata University, Asahimachi-Tohri 1-757, Chuo-ku, Niigata, Niigata 951-8585, Japan.

Wolfgang J Schneider (WJ)

Department of Medical Biochemistry, Max F. Perutz Laboratories, Medical University of Vienna, Vienna 1090, Austria.

Hideaki Bujo (H)

Department of Clinical-Laboratory and Experimental-Research Medicine, Toho University Sakura Medical Center, Shimoshizu 564-1, Sakura, Chiba 285-8741, Japan.

Takashi Miida (T)

Department of Clinical Laboratory Medicine, Juntendo University Graduate School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan; Department of Clinical Laboratory Medicine, Juntendo University School of Medicine, Hongo 2-1-1, Bunkyo-ku, Tokyo 113-8421, Japan.

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Classifications MeSH