Evidence map›Paper›PMID 31626379›Full record

ArticleGlia2020

Galectin-3 modulates postnatal subventricular zone gliogenesis.

Osama Al-Dalahmah, Luana Campos Soares, James Nicholson, Swip Draijer, Mayara Mundim, Victor M Lu, Bin Sun, Teadora Tyler, István Adorján, Eric O'Neill and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  9. Article
  10. Article
  11. Galectins-Potential Therapeutic Targets for Neurodegenerative Disorders.International journal of molecular sciences · 2022
    Review
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  14. Review
  15. Review
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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

11 authors at 3 institutions in 3 countries.

Osama Al-DalahmahDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Luana Campos SoaresDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
James NicholsonDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Swip DraijerDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Mayara MundimDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Victor M LuDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Bin SunDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Teadora TylerDepartment of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
István AdorjánDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Eric O'NeillDepartment of Oncology, University of Oxford, Oxford, UK.
Francis G SzeleDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.ORCID 0000-0002-2931-0673
University of Oxford · GBSemmelweis University · HUColumbia University Irving Medical Center · US

Funding

Biotechnology and Biological Sciences Research Council BB/J018635/1Medical Research Council G1000691Medical Research Council MR/L022656/1
6 · The paper itself

Abstract

Postnatal subventricular zone (SVZ) neural stem cells generate forebrain glia, namely astrocytes and oligodendrocytes. The cues necessary for this process are unclear, despite this phase of brain development being pivotal in forebrain gliogenesis. Galectin-3 (Gal-3) is increased in multiple brain pathologies and thereby regulates astrocyte proliferation and inflammation in injury. To study the function of Gal-3 in inflammation and gliogenesis, we carried out functional studies in mouse. We overexpressed Gal-3 with electroporation and using immunohistochemistry surprisingly found no inflammation in the healthy postnatal SVZ. This allowed investigation of inflammation-independent effects of Gal-3 on gliogenesis. Loss of Gal-3 function via knockdown or conditional knockout reduced gliogenesis, whereas Gal-3 overexpression increased it. Gal-3 overexpression also increased the percentage of striatal astrocytes generated by the SVZ but decreased the percentage of oligodendrocytes. These novel findings were further elaborated with multiple analyses demonstrating that Gal-3 binds to the bone morphogenetic protein receptor one alpha (BMPR1α) and increases bone morphogenetic protein (BMP) signaling. Conditional knockout of BMPR1α abolished the effect of Gal-3 overexpression on gliogenesis. Gain-of-function of Gal-3 is relevant in pathological conditions involving the human forebrain, which is particularly vulnerable to hypoxia/ischemia during perinatal gliogenesis. Hypoxic/ischemic injury induces astrogliosis, inflammation and cell death. We show that Gal-3 immunoreactivity was increased in the perinatal human SVZ and striatum after hypoxia/ischemia. Our findings thus show a novel inflammation-independent function for Gal-3; it is necessary for gliogenesis and when increased in expression can induce astrogenesis via BMP signaling.

Indexed as

AnimalsAstrocytesCell DifferentiationCell MovementCerebral VentriclesGalectin 3Gene Expression RegulationIschemiaLateral VentriclesMice, Inbred C57BLMice, TransgenicNeural Stem CellsNeurogenesisNeurogliaOligodendrogliaGalectin 3electroporationgalectin-3gliogenesissubventricular zone

Identifiers

PMID31626379
PMCPMC6916335
OpenAlexW2980692601

What OpenQuestion holds

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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.