Evidence map›Paper›PMID 23558685›Full record

ArticleThe Journal of biological chemistry2013

Dysferlin regulates cell adhesion in human monocytes.

Antoine de Morrée, Bàrbara Flix, Ivana Bagaric, Jun Wang, Marlinde van den Boogaard, Laure Grand Moursel, Rune R Frants, Isabel Illa, Eduard Gallardo, Rene Toes and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. 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
2.8field-weighted citation impact, top 9% 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, 69 citations in OpenAlex.

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  20. Correction of pseudoexon splicing caused by a novel intronic dysferlin mutation.Annals of clinical and translational neurology · 2019
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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

11 authors at 4 institutions in 2 countries.

Antoine de MorréeDepartment of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Bàrbara FlixServei de Neurologia, Laboratori de Neurologia Experimental, Hospital de la Santa Creu i Sant Pau i Institut de Recerca de HSCSP, Universitat Autònoma de Barcelona and Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 08193 Bellaterra, Spain.
Ivana BagaricDepartment of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Jun WangDepartment of Rheumatology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Marlinde van den BoogaardDepartment of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Laure Grand MourselDepartment of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Rune R FrantsDepartment of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Isabel IllaServei de Neurologia, Laboratori de Neurologia Experimental, Hospital de la Santa Creu i Sant Pau i Institut de Recerca de HSCSP, Universitat Autònoma de Barcelona and Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 08193 Bellaterra, Spain.
Eduard GallardoServei de Neurologia, Laboratori de Neurologia Experimental, Hospital de la Santa Creu i Sant Pau i Institut de Recerca de HSCSP, Universitat Autònoma de Barcelona and Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), 08193 Bellaterra, Spain.
Rene ToesDepartment of Rheumatology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Silvère M van der MaarelDepartment of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands. Electronic address: maarel@lumc.nl.
Leiden University Medical Center · NLBiomedical Research Networking Center on Neurodegenerative Diseases · ESCentro de Investigación Biomédica en Red · ESHospital de Sant Pau · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysferlin is mutated in a group of muscular dystrophies commonly referred to as dysferlinopathies. It is highly expressed in skeletal muscle, where it is important for sarcolemmal maintenance. Recent studies show that dysferlin is also expressed in monocytes. Moreover, muscle of dysferlinopathy patients is characterized by massive immune cell infiltrates, and dysferlin-negative monocytes were shown to be more aggressive and phagocytose more particles. This suggests that dysferlin deregulation in monocytes might contribute to disease progression, but the molecular mechanism is unclear. Here we show that dysferlin expression is increased with differentiation in human monocytes and the THP1 monocyte cell model. Freshly isolated monocytes of dysferlinopathy patients show deregulated expression of fibronectin and fibronectin-binding integrins, which is recapitulated by transient knockdown of dysferlin in THP1 cells. Dysferlin forms a protein complex with these integrins at the cell membrane, and its depletion impairs cell adhesion. Moreover, patient macrophages show altered adhesion and motility. These findings suggest that dysferlin is involved in regulating cellular interactions and provide new insight into dysferlin function in inflammatory cells.

Indexed as

Gene Expression RegulationMutationCell AdhesionCell DifferentiationDysferlinHumansImmune SystemInflammationIntegrin beta3MacrophagesMembrane ProteinsMonocytesMuscle ProteinsMuscle, SkeletalMuscular DystrophiesMuscular Dystrophies, Limb-GirdleDysferlinDYSF protein, humanIntegrin beta3Membrane ProteinsMuscle ProteinsCell AdhesionIntegrinMonocytesMuscular DystrophySkeletal Muscle

Identifiers

PMID23558685
PMCPMC3656271
OpenAlexW2021302614

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.