Evidence map›Paper›PMID 29498007›Full record

ArticleMolecular neurobiology2018

Erythropoietin Upregulates Brain Hemoglobin Expression and Supports Neuronal Mitochondrial Activity.

N K Singhal, K Alkhayer, J Shelestak, R Clements, E Freeman, J McDonough

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review).International journal of molecular medicine · 2024
    Review
  8. Article
  9. Review
  10. lncRNA Neat1 regulates neuronal dysfunction post-sepsis via stabilization of hemoglobin subunit beta.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. RNA-Seq analysis of knocking out the neuroprotective proton-sensitive GPR68 on basal and acute ischemia-induced transcriptome changes and signaling in mouse brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. [A review on the relationship between mitochondrial dysfunction and white matter injury in preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Review
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

6 authors at 1 institution in 1 country.

N K SinghalDepartment of Biological Sciences and School of Biomedical Sciences, Kent State University, Kent, OH, 44242, USA. nsingha1@kent.edu.
K AlkhayerDepartment of Biological Sciences and School of Biomedical Sciences, Kent State University, Kent, OH, 44242, USA.
J ShelestakDepartment of Biological Sciences and School of Biomedical Sciences, Kent State University, Kent, OH, 44242, USA.
R ClementsDepartment of Biological Sciences and School of Biomedical Sciences, Kent State University, Kent, OH, 44242, USA.
E FreemanDepartment of Biological Sciences and School of Biomedical Sciences, Kent State University, Kent, OH, 44242, USA.
J McDonoughDepartment of Biological Sciences and School of Biomedical Sciences, Kent State University, Kent, OH, 44242, USA. jmcdonou@kent.edu.
Kent State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a neuro-inflammatory and demyelinating disease. Downregulation of neuronal mitochondrial gene expression and activity have been reported in several studies of MS. We have previously shown that hemoglobin-β (Hbb) signals to the nucleus of neurons and upregulates H3K4me3, a histone mark involved in regulating cellular metabolism and differentiation. The present study was undertaken to evaluate the effect of erythropoietin (EPO) on the upregulation of hemoglobin and mitochondrial-associated neuroprotection. We found that administering EPO (5000 IU/kg intraperitoneally) to mice upregulated brain Hbb expression, levels of H3K4me3, expression of mitochondrial complex III, complex V, and mitochondrial respiration. We also found that the neuronal mitochondrial metabolite N-acetylaspartate (NAA), a marker of neuronal mitochondrial activity, was increased with EPO treatment. Further, we measured the effects of EPO on preventing mitochondrial deficits in the cuprizone toxic demyelinating mouse model of MS. We found that EPO prevented cuprizone-mediated decreases in Hbb, complex III, and NAA. Our data suggest that EPO mediated regulation of Hbb supports neuronal energetics and may provide neuroprotection in MS and other neurodegenerative diseases where a dysfunction of mitochondria contributes to disease.

Indexed as

AnimalsAspartic AcidBrainCell RespirationCuprizoneDisease Models, AnimalElectron Transport Complex IIIErythropoietinHemoglobinsHistonesLysineMaleMethylationMice, Inbred C57BLMitochondriaModels, BiologicalAspartic AcidCuprizoneElectron Transport Complex IIIErythropoietinHemoglobinsHistonesLysineMyelin Basic ProteinN-acetylaspartateErythropoietinH3K4me3HemoglobinMitochondriaMultiple sclerosisN-acetylaspartate

Identifiers

PMID29498007
OpenAlexW2789856325

What OpenQuestion holds

Textmetadata
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.