Evidence map›Paper›PMID 9588880›Full record

ArticleThe American journal of pathology1998

Activated keratinocytes in the epidermis of hypertrophic scars.

M Machesney, N Tidman, A Waseem, L Kirby, I Leigh

Abstract read
In one paragraph

Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.1field-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

43 citing papers in PubMed, 160 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Transcriptomic Differences Between Immortalized Oral and Skin Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Keratin isoform shifts modulate motility signals during wound healing.bioRxiv : the preprint server for biology · 2024
    Article
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  10. Review
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  12. Article
  13. Review
  14. Article
  15. Exploratory Genome-Wide Interaction Analysis of Nonsteroidal Anti-inflammatory Drugs and Predicted Gene Expression on Colorectal Cancer Risk.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
  16. Article
  17. Article
  18. Vestibulovaginal Sclerosis Versus Lichen Sclerosus.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2018
    Article
  19. Article
  20. Scar formation following excisional and burn injuries in a red Duroc pig model.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2017
    Article
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 1 institution in 1 country.

M MachesneyCentre for Cutaneous Research, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, United Kingdom.
N Tidman
A Waseem
L Kirby
I Leigh
Queen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of hypertrophic scarring, a pathological end point of wound healing, is unknown. The scars most commonly occur when epithelialization has been delayed during, for example, the healing of deep dermal burn wounds. Hypertrophic scars are conventionally described as a dermal pathology in which the epidermis has only a passive role. In this study, the expression of keratin intermediate filament proteins and filaggrin has been investigated in the epidermis of hypertrophic scars and site-matched controls from the same patients. Hypertrophic scar epidermis was found to express the hyperproliferative keratins K6 and K16 in interfollicular epidermis in association with K17 and precocious expression of filaggrin. K16 mRNA was localized by in situ hybridization using a highly specific cRNA probe. In contrast to the immunohistochemical location of K16 protein, the K16 mRNA was found to be expressed in the basal cell layer of normal skin. In hypertrophic scars the mRNA distribution corroborated the abnormal K16 protein distribution. These results suggest the keratinocytes in hypertrophic scar epidermis have entered an alternative differentiation pathway and are expressing an activated phenotype. Activated keratinocytes are a feature of the early stages of wound healing producing growth factors that influence fibroblasts, endothelial cells, and the inflammatory response. We propose that cellular mechanisms in the pathogenesis of hypertrophic scarring are more complex than isolated dermal phenomena. The persistence of activated keratinocytes in hypertrophic scar epidermis implicates abnormal epidermal-mesenchymal interactions.

Indexed as

AdultAgedAnimalsAntibodies, MonoclonalCell DifferentiationChildChild, PreschoolCicatrix, HypertrophicDNA PrimersEpidermisFemaleFilaggrin ProteinsHumansImmunohistochemistryIn Situ Hybridization, FluorescenceIntermediate Filament ProteinsAntibodies, MonoclonalDNA PrimersFilaggrin ProteinsFLG protein, humanIntermediate Filament ProteinsKeratinsRNA, Messenger

Identifiers

PMID9588880
PMCPMC1858601
OpenAlexW1958586460

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.