Evidence map›Paper›PMID 31945017›Full record

ArticleThe Journal of clinical investigation2020

Profilin 1 delivery tunes cytoskeletal dynamics toward CNS axon regeneration.

Rita Pinto-Costa, Sara C Sousa, Sérgio C Leite, Joana Nogueira-Rodrigues, Tiago Ferreira da Silva, Diana Machado, Joana Marques, Ana Catarina Costa, Márcia A Liz, Francesca Bartolini and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

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  13. Profilin affects microtubule dynamics via actin.The Journal of cell biology · 2024
    Article
  14. Article
  15. Article
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  17. The loss of profilin1 is catastrophic to podocytes.The Journal of clinical investigation · 2023
    Article
  18. Article
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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

14 authors at 6 institutions in 4 countries.

Rita Pinto-CostaNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Sara C SousaNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Sérgio C LeiteNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Joana Nogueira-RodriguesNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Tiago Ferreira da SilvaNeuroLipid Biology Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, Universidade do Porto, Porto, Portugal.
Diana MachadoNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Joana MarquesNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Ana Catarina CostaNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Márcia A LizNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Francesca BartoliniDepartment of Pathology and Cell Biology, Columbia University, New York, New York, USA.
Pedro BritesNeuroLipid Biology Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, Universidade do Porto, Porto, Portugal.
Mercedes CostellDepartment of Biochemistry and Molecular Biology and Estructura de Reserca Interdisciplinar en Biotecnologia i Biomedicina, Universitat de València, Valencia, Spain.
Reinhard FässlerDepartment of Molecular Medicine, Max Plank Institute of Biochemistry, Martinsried, Germany.
Mónica M SousaNerve Regeneration Group, Program in Neurobiology and Neurologic Disorders, Instituto de Biologia Molecular e Celular (IBMC) and Instituto de Inovação e Investigação em Saúde, and.
Instituto de Biologia Molecular e CelularUniversidade do Porto · PTi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTColumbia University · USInstituto de Biomedicina de Valencia · ESMax Planck Institute of Biochemistry · DE

Funding

Pathogenic Roles for Microtubule Stabilization Pathways in Alzheimers diseaseR01AG050658 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Francesca Bartolini · 2016 to 2026
$3.5M
NIA NIH HHS R01 AG050658
6 · The paper itself

Abstract

After trauma, regeneration of adult CNS axons is abortive, causing devastating neurologic deficits. Despite progress in rehabilitative care, there is no effective treatment that stimulates axonal growth following injury. Using models with different regenerative capacities, followed by gain- and loss-of-function analysis, we identified profilin 1 (Pfn1) as a coordinator of actin and microtubules (MTs), powering axonal growth and regeneration. In growth cones, Pfn1 increased actin retrograde flow, MT growth speed, and invasion of filopodia by MTs, orchestrating cytoskeletal dynamics toward axonal growth. In vitro, active Pfn1 promoted MT growth in a formin-dependent manner, whereas localization of MTs to growth cone filopodia was facilitated by direct MT binding and interaction with formins. In vivo, Pfn1 ablation limited regeneration of growth-competent axons after sciatic nerve and spinal cord injury. Adeno-associated viral (AAV) delivery of constitutively active Pfn1 to rodents promoted axonal regeneration, neuromuscular junction maturation, and functional recovery of injured sciatic nerves, and increased the ability of regenerating axons to penetrate the inhibitory spinal cord glial scar. Thus, we identify Pfn1 as an important regulator of axonal regeneration and suggest that AAV-mediated delivery of constitutively active Pfn1, together with the identification of modulators of Pfn1 activity, should be considered to treat the injured nervous system.

Indexed as

CytoskeletonGenetic TherapyNerve RegenerationSpinal Cord InjuriesAnimalsDependovirusGrowth ConesMiceMice, KnockoutNeuromuscular JunctionProfilinsSciatic NerveTransduction, GeneticPfn1 protein, mouseProfilinsCell BiologyCytoskeletonNeuroscience

Identifiers

PMID31945017
PMCPMC7108904
OpenAlexW2999116629

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.