Evidence map›Paper›PMID 30477489›Full record

ArticleBMC biology2018

Migration through a small pore disrupts inactive chromatin organization in neutrophil-like cells.

Elsie C Jacobson, Jo K Perry, David S Long, Ada L Olins, Donald E Olins, Bryon E Wright, Mark H Vickers, Justin M O'Sullivan

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

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  19. How the chromatin landscape influences nuclear morphology.Frontiers in cell and developmental biology · 2025
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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

8 authors at 2 institutions in 2 countries.

Elsie C JacobsonLiggins Institute, University of Auckland, Auckland, New Zealand.
Jo K PerryLiggins Institute, University of Auckland, Auckland, New Zealand.
David S LongAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Ada L OlinsCollege of Pharmacy, Department of Pharmaceutical Sciences, University of New England, Portland, ME, USA.
Donald E OlinsCollege of Pharmacy, Department of Pharmaceutical Sciences, University of New England, Portland, ME, USA.
Bryon E WrightAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Mark H VickersLiggins Institute, University of Auckland, Auckland, New Zealand.
Justin M O'SullivanLiggins Institute, University of Auckland, Auckland, New Zealand. justin.osullivan@auckland.ac.nz.ORCID 0000-0003-2927-450X
University of Auckland · NZNew England College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMammalian cells are flexible and can rapidly change shape when they contract, adhere, or migrate. The nucleus must be stiff enough to withstand cytoskeletal forces, but flexible enough to remodel as the cell changes shape. This is particularly important for cells migrating through confined spaces, where the nuclear shape must change in order to fit through a constriction. This occurs many times in the life cycle of a neutrophil, which must protect its chromatin from damage and disruption associated with migration. Here we characterized the effects of constricted migration in neutrophil-like cells.

resultsTotal RNA sequencing identified that migration of neutrophil-like cells through 5- or 14-μm pores was associated with changes in the transcript levels of inflammation and chemotaxis-related genes when compared to unmigrated cells. Differentially expressed transcripts specific to migration with constriction were enriched for groups of genes associated with cytoskeletal remodeling. Hi-C was used to capture the genome organization in control and migrated cells. Limited switching was observed between the active (A) and inactive (B) compartments after migration. However, global depletion of short-range contacts was observed following migration with constriction compared to migration without constriction. Regions with disrupted contacts, TADs, and compartments were enriched for inactive chromatin.

conclusionShort-range genome organization is preferentially altered in inactive chromatin, possibly protecting transcriptionally active contacts from the disruptive effects of migration with constriction. This is consistent with current hypotheses implicating heterochromatin as the mechanoresponsive form of chromatin. Further investigation concerning the contribution of heterochromatin to stiffness, flexibility, and protection of nuclear function will be important for understanding cell migration in relation to human health and disease.

Indexed as

Cell NucleusChromatinHL-60 CellsHumansNeutrophilsChromatinChromatin conformationEpigeneticsHeterochromatinHi-CImmuneMechanotransductionMigrationNeutrophilNuclear remodelingTranscription

Identifiers

PMID30477489
PMCPMC6257957
OpenAlexW2950549058

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.