Evidence map›Paper›PMID 37905100›Full record

ArticlebioRxiv : the preprint server for biology2023

Inflammatory stress-mediated chromatin changes underlie dysfunction in endothelial cells.

Haibo Liu, Amada D Caliz, Heather Learnard, Milka Koupenova, John F Keaney, Shashi Kant, Lihua Julie Zhu, Anastassiia Vertii

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Haibo LiuMolecular, Cell and Cancer Biology Department, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Amada D CalizDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Heather LearnardCardiovascular Medicine, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Milka KoupenovaCardiovascular Medicine, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, USA.
John F KeaneyDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Shashi KantDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Lihua Julie ZhuMolecular, Cell and Cancer Biology Department, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Anastassiia VertiiMolecular, Cell and Cancer Biology Department, University of Massachusetts Chan Medical School, Worcester, MA, USA.

Funding

Telomerase Reverse Transcriptase in Vascular HomeostasisR01HL151626 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI KEANEY, JOHN FRANCIS · 2020 to 2023
$2.4M
Mixed Lineage Kinase 2 (MLK2) and vascular homeostasisR03TR004452 · NCATS · BRIGHAM AND WOMEN'S HOSPITAL · PI KANT, SHASHI · 2023 to 2023
$173k
NCATS NIH HHS R03 TR004452NHLBI NIH HHS R01 HL151626
6 · The paper itself

Abstract

Inflammatory stresses underlie endothelial dysfunction and contribute to the development of chronic cardiovascular disorders such as atherosclerosis and vascular fibrosis. The initial transcriptional response of endothelial cells to pro-inflammatory cytokines such as TNF-alpha is well established. However, very few studies uncover the effects of inflammatory stresses on chromatin architecture. We used integrative analysis of ATAC-seq and RNA-seq data to investigate chromatin alterations in human endothelial cells in response to TNF-alpha and febrile-range heat stress exposure. Multi-omics data analysis suggests a correlation between the transcription of stress-related genes and endothelial dysfunction drivers with chromatin regions exhibiting differential accessibility. Moreover, microscopy identified the dynamics in the nuclear organization, specifically, the changes in a subset of heterochromatic nucleoli-associated chromatin domains, the centromeres. Upon inflammatory stress exposure, the centromeres decreased association with nucleoli in a p38-dependent manner and increased the number of transcripts from pericentromeric regions. Overall, we provide two lines of evidence that suggest chromatin alterations in vascular endothelial cells during inflammatory stresses.

Indexed as

centromereschromatincytokinesfebrileheat stressheterochromatininflammationstressTNF-alphavascular endothelial cells

Identifiers

PMID37905100
PMCPMC10614786

What OpenQuestion holds

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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.