Evidence map›Paper›PMID 22521588›Full record

ArticleNeuroscience2012

miR-32 and its target SLC45A3 regulate the lipid metabolism of oligodendrocytes and myelin.

D Shin, S Y B Howng, L J Ptáček, Y-H Fu

Abstract read
In one paragraph

Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

36 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The epigenetic landscape of oligodendrocyte lineage cells.Annals of the New York Academy of Sciences · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Melanosome Biogenesis in the Pigmentation of Mammalian Skin.Integrative and comparative biology · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. MS CD49dCells · 2019
    Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

D ShinDepartment of Neurology, University of California San Francisco, 1550 Fourth Street, San Francisco, CA 94158, USA.
S Y B Howng
L J Ptáček
Y-H Fu
University of California, San Francisco · US

Funding

Molecular Basis of the Demylinating Disorder ADLDR01NS041331 · NINDS · UNIVERSITY OF UTAH · PI FU, YING-HUI · 2001 to 2003
$1.0M
The role of Lamin B1 in myelin maintenance and demyelinationR01NS062733 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FU, YING-HUI · 2009 to 2010
$850k
Howard Hughes Medical InstituteNINDS NIH HHS NS062733NINDS NIH HHS R01 NS041331NINDS NIH HHS R01 NS062733
6 · The paper itself

Abstract

Oligodendrocytes generate large amounts of myelin by extension of their cell membranes. Though lipid is the major component of myelin, detailed lipid metabolism in the maintenance of myelin is not understood. We reported previously that miR-32 might be involved in myelin maintenance (Shin et al., 2009). Here we demonstrate a novel role for miR-32 in oligodendrocyte function and development through the regulation of SLC45A3 (solute carrier family 45, member 3) and other downstream targets such as CLDN-11. miR-32 is highly expressed in the myelin-enriched regions of the brain and mature oligodendrocytes, and it promotes myelin protein expression. We found that miR-32 directly regulates the expression of SLC45A3 by binding to the complementary sequence on the 3'UTR of cldn11 and slc45a3. As a myelin-enriched putative sugar transporter, SLC45A3 enhances intracellular glucose levels and the synthesis of long-chain fatty acids. Therefore, overexpression of SLC45A3 triggers neutral lipid accumulation. Interestingly, both overexpression and suppression of SLC45A3 reduces myelin protein expression in mature oligodendrocytes and alters oligodendrocyte morphology, indicating that tight regulation of SLC45A3 expression is necessary for the proper maintenance of myelin proteins and structure. Taken together, our data suggest that miR-32 and its downstream target SLC45A3 play important roles in myelin maintenance by modulating glucose and lipid metabolism and myelin protein expression in oligodendrocytes.

Indexed as

AnimalsBlotting, WesternGene Expression RegulationImmunohistochemistryIn Situ HybridizationLipid MetabolismMembrane Transport ProteinsMiceMice, KnockoutMicroRNAsMicroscopy, Electron, TransmissionMonosaccharide Transport ProteinsMutagenesis, Site-DirectedMyelin SheathOligodendrogliaReal-Time Polymerase Chain ReactionMembrane Transport ProteinsMicroRNAsMIRN32 microRNA, mouseMonosaccharide Transport ProteinsSLC45A3 protein, mouse

Identifiers

PMID22521588
PMCPMC3370422
OpenAlexW2088152440

What OpenQuestion holds

Textmetadata
LicenceTDM
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.