Evidence map›Paper›PMID 32012800›Full record

ArticleInternational journal of molecular sciences2020

Myoblast Migration and Directional Persistence Affected by Syndecan-4-Mediated Tiam-1 Expression and Distribution.

Daniel Becsky, Szuzina Gyulai-Nagy, Arpad Balind, Peter Horvath, Laszlo Dux, Aniko Keller-Pinter

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  9. Rac1, A Potential Target for Tumor Therapy.Frontiers in oncology · 2021
    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

6 authors at 2 institutions in 1 country.

Daniel BecskyDepartment of Biochemistry, Faculty of Medicine, University of Szeged, H-6720 Szeged, Hungary.
Szuzina Gyulai-NagyDepartment of Biochemistry, Faculty of Medicine, University of Szeged, H-6720 Szeged, Hungary.
Arpad BalindInstitute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, H-6726 Szeged, Hungary.
Peter HorvathInstitute of Biochemistry, Biological Research Centre, Hungarian Academy of Sciences, H-6726 Szeged, Hungary.
Laszlo DuxDepartment of Biochemistry, Faculty of Medicine, University of Szeged, H-6720 Szeged, Hungary.
Aniko Keller-PinterDepartment of Biochemistry, Faculty of Medicine, University of Szeged, H-6720 Szeged, Hungary.
University of Szeged · HUHUN-REN Szegedi Biológiai Kutatóközpont · HU

Funding

Emberi Eroforrások Minisztériuma EMMI:13725-2/2018/INTFINEuropean Regional Development Funds GINOP-2.3.2-15-2016-00006European Regional Development Funds GINOP-2.3.2-15-2016-00026 and GINOP-2.3.2-15-2016-00037János Bolyai Research Scholarship of the Hungarian Academy of Sciences to Aniko Keller-PinterLENDULET-BIOMAG Grant 2018-342Nemzeti Kutatási, Fejlesztési és Innovaciós Alap UNKP-19-4-SZTE-23Nemzeti Kutatási Fejlesztési és Innovációs Hivatal EFOP-3.6.2-16-2017-00006Nemzeti Kutatási Fejlesztési és Innovációs Hivatal GINOP-2.3.2-15-2016-00040 (MYOTeam)University of Szeged University of Szeged Open Access Fund, Hungary
6 · The paper itself

Abstract

Skeletal muscle is constantly renewed in response to injury, exercise, or muscle diseases. Muscle stem cells, also known as satellite cells, are stimulated by local damage to proliferate extensively and form myoblasts that then migrate, differentiate, and fuse to form muscle fibers. The transmembrane heparan sulfate proteoglycan syndecan-4 plays multiple roles in signal transduction processes, such as regulating the activity of the small GTPase Rac1 (Ras-related C3 botulinum toxin substrate 1) by binding and inhibiting the activity of Tiam1 (T-lymphoma invasion and metastasis-1), a guanine nucleotide exchange factor for Rac1. The Rac1-mediated actin remodeling is required for cell migration. Syndecan-4 knockout mice cannot regenerate injured muscle; however, the detailed underlying mechanism is unknown. Here, we demonstrate that shRNA-mediated knockdown of syndecan-4 decreases the random migration of mouse myoblasts during live-cell microscopy. Treatment with the Rac1 inhibitor NSC23766 did not restore the migration capacity of syndecan-4 silenced cells; in fact, it was further reduced. Syndecan-4 knockdown decreased the directional persistence of migration, abrogated the polarized, asymmetric distribution of Tiam1, and reduced the total Tiam1 level of the cells. Syndecan-4 affects myoblast migration via its role in expression and localization of Tiam1; this finding may facilitate greater understanding of the essential role of syndecan-4 in the development and regeneration of skeletal muscle.

Indexed as

Cell MovementGene Expression RegulationAnimalsCell LineGene Knockdown TechniquesMiceMyoblastsSyndecan-4T-Lymphoma Invasion and Metastasis-inducing Protein 1Sdc4 protein, mouseSyndecan-4Tiam1 protein, mouseT-Lymphoma Invasion and Metastasis-inducing Protein 1cell migrationdirectional persistencemuscle regenerationmyoblastNSC23766proteoglycanRac1skeletal musclesyndecan-4Tiam1

Identifiers

PMID32012800
PMCPMC7037462
OpenAlexW3002855617

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.