Evidence map›Paper›PMID 27541284›Full record

ArticleMolecular neurobiology2017

Neuroprotection and CD131/GDNF/AKT Pathway of Carbamylated Erythropoietin in Hypoxic Neurons.

Jing Ding, Jing Wang, Qin-Ying Li, Jie-Zhong Yu, Cun-Gen Ma, Xin Wang, Chuan-Zhen Lu, Bao-Guo Xiao

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The Development of Novel Drug Treatments for Stroke Patients: A Review.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

8 authors at 4 institutions in 1 country.

Jing DingDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Jing WangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Qin-Ying LiInstitute of Neurology, Huashan Hospital, Institute of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, 12 Middle Wulumuqi Road, Shanghai, 200040, China.
Jie-Zhong YuInstitute of Brain Science, Shanxi Datong University, Shanxi, 037009, China.
Cun-Gen MaInstitute of Brain Science, Shanxi Datong University, Shanxi, 037009, China.
Xin WangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, China.
Chuan-Zhen LuInstitute of Neurology, Huashan Hospital, Institute of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, 12 Middle Wulumuqi Road, Shanghai, 200040, China.
Bao-Guo XiaoInstitute of Neurology, Huashan Hospital, Institute of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, 12 Middle Wulumuqi Road, Shanghai, 200040, China. bgxiao@shmu.edu.cn.
Fudan University · CNShanxi Datong University · CNZhongshan Hospital · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carbamylated erythropoietin (CEPO), an EPO derivative, is attracting widespread interest due to neuroprotective effects without erythropoiesis. However, little is known about molecular mechanisms behind CEPO-mediated neuroprotection. In primary neurons with oxygen-glucose deprivation (OGD) and mice with hypoxia-reoxygenation, the neuroprotection and possible molecular mechanism of CEPO were performed by immunohistochemistry and immunocytochemistry, Western blot, RT-PCR, and ELISA. The comparisons were analyzed by ANOVA followed by unpaired two-tailed Student's t test. Both CEPO and EPO showed the neuroprotective effects in OGD model and hypoxic brain. CEPO did not trigger JAK-2 but activated AKT through glial cell line-derived neurotrophic factor (GDNF). It has been shown that CEPO acts upon a heteroreceptor complex comprising both the EPO receptor and the common β receptor subunit (βcR, also known as CD131). The blockage of CD131 reduced CEPO-mediated GDNF production, while GFR receptor blockage and GDNF neutralization inhibited CEPO-induced neurogenesis. Addition of GDNF to cultured neurons increased phosphorylation of AKT. CEPO protects neurons possible through the CD131/GDNF/AKT pathway.

Indexed as

Signal TransductionAnimalsCytokine Receptor Common beta SubunitErythropoietinFemaleGlial Cell Line-Derived Neurotrophic FactorHypoxiaMice, Inbred C57BLNeuronsNeuroprotectionNeuroprotective AgentsPhosphorylationProto-Oncogene Proteins c-aktcarbamylated erythropoietinCytokine Receptor Common beta SubunitErythropoietinGlial Cell Line-Derived Neurotrophic FactorNeuroprotective AgentsProto-Oncogene Proteins c-aktCarbamylated erythropoietinCD131Glial cell-derived neurotrophic factorNeuroprotection

Identifiers

PMID27541284
OpenAlexW2508956885

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.