Evidence map›Paper›PMID 23638963›Full record

ArticleCNS neuroscience & therapeutics2013

The involvement of programmed cell death 5 (PDCD5) in the regulation of apoptosis in cerebral ischemia/reperfusion injury.

Chun-Hua Chen, Zhao Jiang, Jun-Hao Yan, Lei Yang, Ke Wang, Ying-Yu Chen, Jing-Yan Han, John H Zhang, Chang-Man Zhou

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  4. Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Article
  5. Article
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  8. PDCD5 says no to NO.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Programmed cell death 5 suppresses AKT-mediated cytoprotection of endothelium.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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  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

9 authors at 3 institutions in 2 countries.

Chun-Hua ChenDepartment of Anatomy and Embryology, Peking University Health Science Center, Beijing, China.
Zhao Jiang
Jun-Hao Yan
Lei Yang
Ke Wang
Ying-Yu Chen
Jing-Yan Han
John H Zhang
Chang-Man Zhou
Peking University · CNLoma Linda University · USState Administration of Traditional Chinese Medicine of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsProgrammed Cell Death 5 (PDCD5) is a protein that accelerates apoptosis in different types of cells in response to various stimuli and is down-regulated in many cancer tissues. We hypothesized in this study that down-regulating PDCD5 can protect the brain from ischemic damage by inhibiting PDCD5-induced apoptotic pathway.

methodsOne hundred and sixty male Sprague-Dawley rats were randomly assigned to five groups: Sham surgery (n = 25), MCAO (n = 45), MCAO+rhPDCD5 (RhPDCD5) (n = 30), MCAO+control siRNA (n = 30), and MCAO+PDCD5 siRNA (n = 30). At 24 h following MCAO, immunohistochemistry and Western blot were performed.

resultsPDCD5 siRNA reduced the infarct volume, improved neurological deficits, improved cerebral blood flow (CBF), and reduced Evans blue extravasation. Meanwhile, over-expression of PDCD5 protein with recombinant human PDCD5 (rhPDCD5) had an opposite effect. Immunohistochemistry and Western blot demonstrated PDCD5 siRNA decreased the expressions of key proapoptotic proteins such as p53, Bax/Bcl-2, and cleaved caspase-3 in the penumbra areas, whereas rhPDCD5 increased cell apoptosis. Double fluorescence labeling showed the positive immunoreactive materials of PDCD5 were partly colocalized with MAP2, GFAP, CD34, p53, and caspase-3 in the penumbra areas in brain.

conclusionsPDCD5-induced apoptosis and over-expression of PDCD5 are harmful to the ischemic neurons in vivo. Meanwhile, the inhibition of PDCD5 may be protective via reducing the apoptotic-related protein such as p53, Bax, and caspase-3. This observation may have potential for the treatment of ischemic cerebral stroke.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBrain IschemiaHumansMaleNeoplasm ProteinsNeuronsRandom AllocationRatsRats, Sprague-DawleyReperfusion InjuryApoptosis Regulatory ProteinsNeoplasm ProteinsPDCD5 protein, humanApoptosisMCAOPDCD5siRNA in vivo

Identifiers

PMID23638963
PMCPMC6493388
OpenAlexW2074819857

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.