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Erythropoietin reduces experimental autoimmune encephalomyelitis severity via neuroprotective mechanisms

Overview of attention for article published in Journal of Neuroinflammation, October 2017
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Title
Erythropoietin reduces experimental autoimmune encephalomyelitis severity via neuroprotective mechanisms
Published in
Journal of Neuroinflammation, October 2017
DOI 10.1186/s12974-017-0976-5
Pubmed ID
Authors

M. Moransard, M. Bednar, K. Frei, M. Gassmann, O. O. Ogunshola

Abstract

Treatment with erythropoietin (Epo) in experimental autoimmune encephalomyelitis (EAE), the rodent model of multiple sclerosis (MS), has consistently been shown to ameliorate disease progression and improve overall outcome. The effect has been attributed to modulation of the immune response and/or preservation of the central nervous system (CNS) tissue integrity. It remains unclear, however, if (a) Epo acts primarily in the CNS or the periphery and if (b) Epo's beneficial effect in EAE is mainly due to maintaining CNS tissue integrity or to modulation of the immune response. If Epo acts primarily by modulating the immune system, where is this modulation required? In the periphery, the CNS or both? To address these questions, we used two well-characterized transgenic mouse strains that constitutively overexpress recombinant human Epo (rhEpo) either systemically (tg6) or in CNS only (tg21) in a MOG-induced EAE model. We assessed clinical severity, disease progression, immunomodulation, and CNS tissue integrity, including neuronal survival. Although disease onset remained unaffected, EAE progression was alleviated in transgenic animals compared to controls with both lines performing equally well showing that expression of Epo in the periphery is not required; Epo expression in the CNS is sufficient. Immunomodulation was observed in both strains but surprisingly the profile of modulation differed substantially between strains. Modulation in the tg21 strain was limited to a reduction in macrophages in the CNS, with no peripheral immunomodulatory effects observed. In contrast, in the tg6 strain, macrophages were upregulated in the CNS, and, in the periphery of this strain, T cells and macrophages were downregulated. The lack of a consistent immunomodulatory profile across both transgenic species suggests that immunomodulation by Epo is unlikely to be the primary mechanism driving amelioration of EAE. Finally, CNS tissue integrity was affected in all strains. Although myelin appeared equally damaged in all strains, neuronal survival was significantly improved in the spinal cord of tg21 mice, indicating that Epo may ameliorate EAE predominantly by protecting neurons. Our data suggests that moderate elevated brain Epo levels provide clinically significant neuroprotection in EAE without modulation of the immune response making a significant contribution.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 43 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 43 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 19%
Student > Ph. D. Student 7 16%
Student > Bachelor 6 14%
Other 6 14%
Student > Master 3 7%
Other 7 16%
Unknown 6 14%
Readers by discipline Count As %
Medicine and Dentistry 10 23%
Neuroscience 5 12%
Biochemistry, Genetics and Molecular Biology 4 9%
Veterinary Science and Veterinary Medicine 2 5%
Nursing and Health Professions 2 5%
Other 11 26%
Unknown 9 21%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 07 June 2018.
All research outputs
#15,792,432
of 25,002,204 outputs
Outputs from Journal of Neuroinflammation
#1,768
of 2,893 outputs
Outputs of similar age
#187,975
of 331,594 outputs
Outputs of similar age from Journal of Neuroinflammation
#16
of 46 outputs
Altmetric has tracked 25,002,204 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,893 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.7. This one is in the 35th percentile – i.e., 35% of its peers scored the same or lower than it.
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 331,594 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 46 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 63% of its contemporaries.