Evidence map›Paper›PMID 31358730›Full record

ArticleCell death & disease2019

Modifying PTEN recruitment promotes neuron survival, regeneration, and functional recovery after CNS injury.

Alireza Pirsaraei Shabanzadeh, Philippe Matteo D'Onofrio, Mark Magharious, Kyung An Brian Choi, Philippe Patrick Monnier, Paulo Dieter Koeberle

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Molecular mechanisms of exercise contributing to tissue regeneration.Signal transduction and targeted therapy · 2022
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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

6 authors at 2 institutions in 1 country.

Alireza Pirsaraei ShabanzadehDivision of Anatomy, Department of Surgery, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Philippe Matteo D'OnofrioDivision of Anatomy, Department of Surgery, University of Toronto, Toronto, ON, M5S 1A8, Canada.ORCID http://orcid.org/0000-0002-1957-2100
Mark MaghariousDivision of Anatomy, Department of Surgery, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Kyung An Brian ChoiDivision of Anatomy, Department of Surgery, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Philippe Patrick MonnierDepartments of Physiology, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Paulo Dieter KoeberleDivision of Anatomy, Department of Surgery, University of Toronto, Toronto, ON, M5S 1A8, Canada. paulo.koeberle@utoronto.ca.
University of Toronto · CAUniversity Health Network · CA

Funding

CIHR MOP 119309
6 · The paper itself

Abstract

Phosphatase and tensin homolog (PTEN) regulates apoptosis and axonal growth in the developing and adult central nervous system (CNS). Here, we show that human PTEN C-terminal PDZ interactions play a critical role in neuronal apoptosis and axon regeneration after traumatic CNS injury and stroke, highlighted by the findings that antagonizing the PDZ-motif interactions of PTEN has therapeutic applicability for these indications. Interestingly, the death-inducing function of PTEN following ischemic insult depends on a PDZ-domain interaction with MAGI-2 and MAST205, PDZ proteins that are known to recruit PTEN to the plasma membrane and stabilize its interaction with PIP3. Treatments with a human peptide that prevents PTEN association with MAGI-2 or MAST205 increased neuronal survival in multiple stroke models, in vitro. A pro-survival effect was also observed in models of retinal ischemia, optic nerve transection, and after middle cerebral artery occlusion (MCAO) in adult rats. The human PTEN peptide also improved axonal regeneration in the crushed optic nerve. Furthermore, human PTEN peptide therapy promoted functional improvement after MCAO or retinal ischemia induced via ophthalmic artery ligation. These findings show that the human peptide-based targeting of C-terminal PTEN PDZ interactions has therapeutic potential for insults of the CNS, including trauma and stroke.

Indexed as

Amino Acid SequenceAnimalsAxonsCell SurvivalDisease Models, AnimalExerciseFemaleHEK293 CellsHumansInfarction, Middle Cerebral ArteryMitogen-Activated Protein KinasesNerve RegenerationNeuroprotective AgentsOptic NerveOptic Nerve InjuriesPDZ DomainsMitogen-Activated Protein KinasesNeuroprotective AgentsPeptidesPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePTEN protein, humanPten protein, rat

Identifiers

PMID31358730
PMCPMC6662832
OpenAlexW2964762750

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.