Evidence map›Paper›PMID 27406993›Full record

ArticleJournal of leukocyte biology2016

Class 3 semaphorins induce F-actin reorganization in human dendritic cells: Role in cell migration.

Sabrina Curreli, Bin Sheng Wong, Olga Latinovic, Konstantinos Konstantopoulos, Nicholas M Stamatos

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. 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
2.3field-weighted citation impact, top 13% 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, 40 citations in OpenAlex.

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  15. Article
  16. Semaphorin3E/plexinD1 Axis in Asthma: What We Know So Far!Advances in experimental medicine and biology · 2021
    Article
  17. Review
  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

5 authors at 3 institutions in 1 country.

Sabrina CurreliInstitute of Human Virology, University of Maryland Medical Center, Baltimore, Maryland, USA.
Bin Sheng WongDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Olga LatinovicInstitute of Human Virology, University of Maryland Medical Center, Baltimore, Maryland, USA.
Konstantinos KonstantopoulosDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Nicholas M StamatosInstitute of Human Virology, University of Maryland Medical Center, Baltimore, Maryland, USA; nstamatos@ihv.umaryland.edu.
Johns Hopkins University · USUniversity of Maryland Medical Center · USUniversity of Maryland, Baltimore · US

Funding

Role of Cellular Sialidase in Pathogenesis of HIV-1K08HL072176 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STAMATOS, NICHOLAS MILTON · 2002 to 2004
$467k
NHLBI NIH HHS K08 HL072176
6 · The paper itself

Abstract

Class 3 semaphorins (Semas) are soluble proteins that are well recognized for their role in guiding axonal migration during neuronal development. In the immune system, Sema3A has been shown to influence murine dendritic cell (DC) migration by signaling through a neuropilin (NRP)-1/plexin-A1 coreceptor axis. Potential roles for class 3 Semas in human DCs have yet to be described. We tested the hypothesis that Sema3A, -3C, and -3F, each with a unique NRP-1 and/or NRP-2 binding specificity, influence human DC migration. In this report, we find that although NRP-1 and NRP-2 are expressed in human immature DCs (imDCs), NRP-2 expression increases as cells mature further, whereas expression of NRP-1 declines dramatically. Elevated levels of RNA encoding plexin-A1 and -A3 are present in both imDCs and mature DC (mDCs), supporting the relevance of Sema/NRP/plexin signaling pathways in these cells. Sema3A, -3C, and -3F bind to human DCs, with Sema3F binding predominantly through NRP-2. The binding of these Semas leads to reorganization of actin filaments at the plasma membrane and increased transwell migration in the absence or presence of chemokine CCL19. Microfluidic chamber assays failed to demonstrate consistent changes in speed of Sema3C-treated DCs, suggesting increased cell deformability as a possible explanation for enhanced transwell migration. Although monocytes express RNA encoding Sema3A, -3C, and -3F, only RNA encoding Sema3C increases robustly during DC differentiation. These data suggest that Sema3A, -3C, and -3F, likely with coreceptors NRP-1, NRP-2, and plexin-A1 and/or -A3, promote migration and possibly other activities of human DCs during innate and adaptive immune responses.

Indexed as

Actin CytoskeletonActinsAdaptive ImmunityCell DifferentiationCells, CulturedChemokine CCL19ChemotaxisCytoskeletonDendritic CellsGene Expression RegulationHumansImmunity, InnateMicrofluidic Analytical TechniquesNerve Tissue ProteinsNeuropilin-1Neuropilin-2ActinsCCL19 protein, humanChemokine CCL19Nerve Tissue ProteinsNeuropilin-1Neuropilin-2neuropilin-2, humanPLXNA1 protein, humanPLXNA2 protein, humanReceptors, Cell SurfaceRecombinant Fusion ProteinsRNA, MessengerSemaphorinschemotaxisneuropilin-1 and -2plexinspolysialic acid

Identifiers

PMID27406993
PMCPMC5109998
OpenAlexW2473177620

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.