Evidence map›Paper›PMID 35851095›Full record

ArticleScientific reports2022

Angiogenic gene characterization and vessel permeability of dermal microvascular endothelial cells isolated from burn hypertrophic scar.

Esteban A Molina, Brandon Hartmann, Mary A Oliver, Liam D Kirkpatrick, John W Keyloun, Lauren T Moffatt, Jeffrey W Shupp, Taryn E Travis, Bonnie C Carney

Abstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
    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

9 authors.

Esteban A MolinaGeorgetown University School of Medicine, Washington, DC, USA.
Brandon HartmannFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
Mary A OliverFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
Liam D KirkpatrickFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
John W KeylounFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
Lauren T MoffattFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
Jeffrey W ShuppFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
Taryn E TravisFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA.
Bonnie C CarneyFirefighter's Burn and Surgical Research Laboratory, MedStar Health Research Institute, 110 Irving Street, NW, GHRB, Room 310, Washington, DC, 20010, USA. bonnie.c.carney@medstar.net.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic scar (HTS) formation is a common challenge for patients after burn injury. Dermal microvascular endothelial cells (DMVECs) are an understudied cell type in HTS. An increase in angiogenesis and microvessel density can be observed in HTS. Endothelial dysfunction may play a role in scar development. This study aims to generate a functional and expression profile of HTS DMVECs. We hypothesize that transcript and protein-level responses in HTS DMVECs differ from those in normal skin (NS). HTSs were created in red Duroc pigs. DMVECs were isolated using magnetic-activated cell sorting with ulex europaeus agglutinin 1 (UEA-1) lectin. Separate transwell inserts were used to form monolayers of HTS DMVECs and NS DMVECs. Cell injury was induced and permeability was assessed. Gene expression in HTS DMVECS versus NS DMVECs was measured. Select differentially expressed genes were further investigated. HTS had an increased area density of dermal microvasculature compared to NS. HTS DMVECs were 17.59% less permeable than normal DMVECs (p < 0.05). After injury, NS DMVECs were 28.4% and HTS DMVECs were 18.8% more permeable than uninjured controls (28.4 ± 4.8 vs 18.8 ± 2.8; p = 0.11). PCR array identified 31 differentially expressed genes between HTS and NS DMVECs, of which 10 were upregulated and 21 were downregulated. qRT-PCR and ELISA studies were in accordance with the array. DMVECs expressed a mixed profile of factors that can contribute to and inhibit scar formation. HTS DMVECs have both a discordant response to cellular insults and baseline differences in function, supporting their proposed role in scar pathology. Further investigation of DMVECs is warranted to elucidate their contribution to HTS pathogenesis.

Indexed as

BurnsCicatrix, HypertrophicAnimalsEndothelial CellsHypertrophyNeovascularization, PathologicPermeabilitySwine

Identifiers

PMID35851095
PMCPMC9293893

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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.