Evidence map›Paper›PMID 34752805›Full record

ArticleJournal of lipid research2022

Loss of ABCA8B decreases myelination by reducing oligodendrocyte precursor cells in mice.

Yiran Liu, David Castano, Francesco Girolamo, Laia Trigueros-Motos, Han-Gyu Bae, Suat Peng Neo, Jeongah Oh, Pradeep Narayanaswamy, Federico Torta, Kerry Anne Rye and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of lipid research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Dyslipidemia is a metabolic hallmark of acute pain in sickle cell disease.medRxiv : the preprint server for health sciences · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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

15 authors at 5 institutions in 4 countries.

Yiran LiuTranslational Laboratories in Genetic Medicine, Agency for Science, Technology and Research, Singapore, Singapore; Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; Cardiovascular Research Institute, National University Health System, Singapore, Singapore.
David CastanoTranslational Laboratories in Genetic Medicine, Agency for Science, Technology and Research, Singapore, Singapore; Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; Cardiovascular Research Institute, National University Health System, Singapore, Singapore.
Francesco GirolamoDepartment of Basic Medical Sciences, Neurosciences, and Sensory Organs, Human Anatomy and Histology Unit, University of Bari School of Medicine, Bari, Italy.
Laia Trigueros-MotosTranslational Laboratories in Genetic Medicine, Agency for Science, Technology and Research, Singapore, Singapore.
Han-Gyu BaeSingapore Bioimaging Consortium, Agency for Science, Technology and Research, Singapore, Singapore.
Suat Peng NeoInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore, Singapore.
Jeongah OhSingapore Lipidomics Incubator, Department of Biochemistry, Life Sciences Institute and Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Pradeep NarayanaswamySingapore Lipidomics Incubator, Department of Biochemistry, Life Sciences Institute and Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Federico TortaSingapore Lipidomics Incubator, Department of Biochemistry, Life Sciences Institute and Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Kerry Anne RyeSchool of Medical Sciences, University of New South Wales, Sydney, Australia.
Dong-Gyu JoSchool of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Jayantha GunaratneInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore, Singapore.
Sangyong JungSingapore Bioimaging Consortium, Agency for Science, Technology and Research, Singapore, Singapore.
Daniela VirgintinoDepartment of Basic Medical Sciences, Neurosciences, and Sensory Organs, Human Anatomy and Histology Unit, University of Bari School of Medicine, Bari, Italy.
Roshni R SingarajaTranslational Laboratories in Genetic Medicine, Agency for Science, Technology and Research, Singapore, Singapore; Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; Cardiovascular Research Institute, National University Health System, Singapore, Singapore. Electronic address: mdcrrs@nus.edu.sg.
Agency for Science, Technology and Research · SGNational University of Singapore · SGUniversity of Bari Aldo Moro · ITSungkyunkwan University · KRUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The myelin sheath, which is wrapped around axons, is a lipid-enriched structure produced by mature oligodendrocytes. Disruption of the myelin sheath is observed in several neurological diseases, such as multiple sclerosis. A crucial component of myelin is sphingomyelin, levels of which can be increased by ABCA8, a member of the ATP-binding cassette transporter family. ABCA8 is highly expressed in the cerebellum, specifically in oligodendroglia. However, whether ABCA8 plays a role in myelination and mechanisms that would underlie this role remain unknown. Here, we found that the absence of Abca8b, a mouse ortholog of ABCA8, led to decreased numbers of cerebellar oligodendrocyte precursor cells (OPCs) and mature oligodendrocytes in mice. We show that in oligodendrocytes, ABCA8 interacts with chondroitin sulfate proteoglycan 4 (CSPG4), a molecule essential for OPC proliferation, migration, and myelination. In the absence of Abca8b, localization of CSPG4 to the plasma membrane was decreased, contributing to reduced cerebellar CSPG4 expression. Cerebellar CSPG4+ OPCs were also diminished, leading to decreased mature myelinating oligodendrocyte numbers and cerebellar myelination levels in Abca8b

Indexed as

ATP-Binding Cassette TransportersMyelin SheathOligodendrocyte Precursor CellsAnimalsCerebellumMiceMice, Inbred C57BLMice, KnockoutOligodendrogliaATP-Binding Cassette TransportersABCA8animal modelsbrain lipidscerebellumcholesterol/traffickingCSPG4hypomyelinationlipid transfer proteinsmyelin disordersmyelin sheath periodicity

Identifiers

PMID34752805
PMCPMC8953628
OpenAlexW3214029468

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.