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Activin receptors regulate the oligodendrocyte lineage in health and disease

Overview of attention for article published in Acta Neuropathologica, February 2018
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (93rd percentile)
  • High Attention Score compared to outputs of the same age and source (85th percentile)

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1 news outlet
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29 X users
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2 patents

Citations

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50 Dimensions

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93 Mendeley
Title
Activin receptors regulate the oligodendrocyte lineage in health and disease
Published in
Acta Neuropathologica, February 2018
DOI 10.1007/s00401-018-1813-3
Pubmed ID
Authors

Alessandra Dillenburg, Graeme Ireland, Rebecca K. Holloway, Claire L. Davies, Frances L. Evans, Matthew Swire, Marie E. Bechler, Daniel Soong, Tracy J. Yuen, Gloria H. Su, Julie-Clare Becher, Colin Smith, Anna Williams, Veronique E. Miron

Abstract

The most prevalent neurological disorders of myelin include perinatal brain injury leading to cerebral palsy in infants and multiple sclerosis in adults. Although these disorders have distinct etiologies, they share a common neuropathological feature of failed progenitor differentiation into myelin-producing oligodendrocytes and lack of myelin, for which there is an unmet clinical need. Here, we reveal that a molecular pathology common to both disorders is dysregulation of activin receptors and that activin receptor signaling is required for the majority of myelin generation in development and following injury. Using a constitutive conditional knockout of all activin receptor signaling in oligodendrocyte lineage cells, we discovered this signaling to be required for myelination via regulation of oligodendrocyte differentiation and myelin compaction. These processes were found to be dependent on the activin receptor subtype Acvr2a, which is expressed during oligodendrocyte differentiation and axonal ensheathment in development and following myelin injury. During efficient myelin regeneration, Acvr2a upregulation was seen to coincide with downregulation of Acvr2b, a receptor subtype with relatively higher ligand affinity; Acvr2b was shown to be dispensable for activin receptor-driven oligodendrocyte differentiation and its overexpression was sufficient to impair the abovementioned ligand-driven responses. In actively myelinating or remyelinating areas of human perinatal brain injury and multiple sclerosis tissue, respectively, oligodendrocyte lineage cells expressing Acvr2a outnumbered those expressing Acvr2b, whereas in non-repairing lesions Acvr2b+ cells were increased. Thus, we propose that following human white matter injury, this increase in Acvr2b expression would sequester ligand and consequently impair Acvr2a-driven oligodendrocyte differentiation and myelin formation. Our results demonstrate dysregulated activin receptor signaling in common myelin disorders and reveal Acvr2a as a novel therapeutic target for myelin generation following injury across the lifespan.

X Demographics

X Demographics

The data shown below were collected from the profiles of 29 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 93 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 93 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 28 30%
Student > Bachelor 10 11%
Researcher 8 9%
Student > Master 8 9%
Other 7 8%
Other 17 18%
Unknown 15 16%
Readers by discipline Count As %
Neuroscience 31 33%
Biochemistry, Genetics and Molecular Biology 14 15%
Medicine and Dentistry 10 11%
Agricultural and Biological Sciences 8 9%
Immunology and Microbiology 2 2%
Other 10 11%
Unknown 18 19%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 34. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 March 2023.
All research outputs
#1,157,919
of 24,987,787 outputs
Outputs from Acta Neuropathologica
#180
of 2,512 outputs
Outputs of similar age
#27,534
of 449,803 outputs
Outputs of similar age from Acta Neuropathologica
#7
of 40 outputs
Altmetric has tracked 24,987,787 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 95th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,512 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 16.4. This one has done particularly well, scoring higher than 92% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 449,803 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 93% of its contemporaries.
We're also able to compare this research output to 40 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 85% of its contemporaries.