Evidence map›Paper›PMID 38479648›Full record

ArticleJournal of lipid research2024

Apolipoprotein A1 and high-density lipoprotein limit low-density lipoprotein transcytosis by binding SR-B1.

Karen Y Y Fung, Tse Wing Winnie Ho, Zizhen Xu, Dante Neculai, Catherine A A Beauchemin, Warren L Lee, Gregory D Fairn

Open access · goldAbstract read
In one paragraph

Article in Journal of lipid research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 18 citations in OpenAlex.

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  8. Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Karen Y Y FungDepartment of Biochemistry, University of Toronto, Toronto, Ontario, Canada; Keenan Research Centre, St. Michael's Hospital, Unity Health Toronto, Toronto, Ontario, Canada.
Tse Wing Winnie HoKeenan Research Centre, St. Michael's Hospital, Unity Health Toronto, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Zizhen XuDepartment of Cell Biology, and Department of Pathology Sir Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Dante NeculaiDepartment of Cell Biology, and Department of Pathology Sir Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Catherine A A BeaucheminDepartment of Physics, Toronto Metropolitan University, Toronto, Ontario, Canada; Interdisciplinary Theoretical and Mathematical Sciences (iTHEMS) program, RIKEN, Wako, Saitama, Japan.
Warren L LeeDepartment of Biochemistry, University of Toronto, Toronto, Ontario, Canada; Keenan Research Centre, St. Michael's Hospital, Unity Health Toronto, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; Interdepartmental Division of Critical Care Medicine, University of Toronto, Toronto, Ontario, Canada. Electronic address: Warren.Lee@unityhealth.to.
Gregory D FairnDepartment of Biochemistry, University of Toronto, Toronto, Ontario, Canada; Keenan Research Centre, St. Michael's Hospital, Unity Health Toronto, Toronto, Ontario, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada; Department of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada. Electronic address: gfairn@dal.ca.
St. Michael's Hospital · CASir Run Run Shaw Hospital · CNRIKEN · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis results from the deposition and oxidation of LDL and immune cell infiltration in the sub-arterial space leading to arterial occlusion. Studies have shown that transcytosis transports circulating LDL across endothelial cells lining blood vessels. LDL transcytosis is initiated by binding to either scavenger receptor B1 (SR-B1) or activin A receptor-like kinase 1 on the apical side of endothelial cells leading to its transit and release on the basolateral side. HDL is thought to partly protect individuals from atherosclerosis due to its ability to remove excess cholesterol and act as an antioxidant. Apolipoprotein A1 (APOA1), an HDL constituent, can bind to SR-B1, raising the possibility that APOA1/HDL can compete with LDL for SR-B1 binding, thereby limiting LDL deposition in the sub-arterial space. To examine this possibility, we used in vitro approaches to quantify the internalization and transcytosis of fluorescent LDL in coronary endothelial cells. Using microscale thermophoresis and affinity capture, we find that SR-B1 and APOA1 interact and that binding is enhanced when using the cardioprotective variant of APOA1 termed Milano (APOA1-Milano). In male mice, transiently increasing the levels of HDL reduced the acute deposition of fluorescently labeled LDL in the atheroprone inner curvature of the aorta. Reduced LDL deposition was also observed when increasing circulating wild-type APOA1 or the APOA1-Milano variant, with a more robust inhibition from the APOA1-Milano. The results suggest that HDL may limit SR-B1-mediated LDL transcytosis and deposition, adding to the mechanisms by which it can act as an atheroprotective particle.

Indexed as

Apolipoprotein A-ILipoproteins, HDLLipoproteins, LDLTranscytosisAnimalsAtherosclerosisEndothelial CellsHumansMaleMiceProtein BindingScavenger Receptors, Class BApoa1 protein, mouseApolipoprotein A-ILipoproteins, HDLLipoproteins, LDLScavenger Receptors, Class Bapolipoprotein A1atherosclerosisHDLLDLtranscytosis

Identifiers

PMID38479648
PMCPMC11004410
OpenAlexW4392723803

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.