Burn eschar stimulates fibroblast and adipose mesenchymal stromal cell proliferation and migration but inhibits endothelial cell sprouting

Hanneke N. Monsuur, Lenie J. van den Broek, Renushka L. Jhingoerie, Adrianus F.P.M. Vloemans, Susan Gibbs

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

The majority of full-thickness burn wounds heal with hypertrophic scar formation. Burn eschar most probably influences early burn wound healing, since granulation tissue only forms after escharotomy. In order to investigate the effect of burn eschar on delayed granulation tissue formation, burn wound extract (BWE) was isolated from the interface between non-viable eschar and viable tissue. The influence of BWE on the activity of endothelial cells derived from dermis and adipose tissue, dermal fibroblasts and adipose tissue-derived mesenchymal stromal cells (ASC) was determined. It was found that BWE stimulated endothelial cell inflammatory cytokine (CXCL8, IL-6 and CCL2) secretion and migration. However, BWE had no effect on endothelial cell proliferation or angiogenic sprouting. Indeed, BWE inhibited basic Fibroblast Growth Factor (bFGF) induced endothelial cell proliferation and sprouting. In contrast, BWE stimulated fibroblast and ASC proliferation and migration. No difference was observed between cells isolated from dermis or adipose tissue. The inhibitory effect of BWE on bFGF-induced endothelial proliferation and sprouting would explain why excessive granulation tissue formation is prevented in full-thickness burn wounds as long as the eschar is still present. Identifying the eschar factors responsible for this might give indications for therapeutic targets aimed at reducing hypertrophic scar formation which is initiated by excessive granulation tissue formation once eschar is removed.

Original languageEnglish
Article number1790
JournalInternational Journal of Molecular Sciences
Volume18
Issue number8
DOIs
Publication statusPublished - 18 Aug 2017

Cite this

Monsuur, Hanneke N. ; van den Broek, Lenie J. ; Jhingoerie, Renushka L. ; Vloemans, Adrianus F.P.M. ; Gibbs, Susan. / Burn eschar stimulates fibroblast and adipose mesenchymal stromal cell proliferation and migration but inhibits endothelial cell sprouting. In: International Journal of Molecular Sciences. 2017 ; Vol. 18, No. 8.
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title = "Burn eschar stimulates fibroblast and adipose mesenchymal stromal cell proliferation and migration but inhibits endothelial cell sprouting",
abstract = "The majority of full-thickness burn wounds heal with hypertrophic scar formation. Burn eschar most probably influences early burn wound healing, since granulation tissue only forms after escharotomy. In order to investigate the effect of burn eschar on delayed granulation tissue formation, burn wound extract (BWE) was isolated from the interface between non-viable eschar and viable tissue. The influence of BWE on the activity of endothelial cells derived from dermis and adipose tissue, dermal fibroblasts and adipose tissue-derived mesenchymal stromal cells (ASC) was determined. It was found that BWE stimulated endothelial cell inflammatory cytokine (CXCL8, IL-6 and CCL2) secretion and migration. However, BWE had no effect on endothelial cell proliferation or angiogenic sprouting. Indeed, BWE inhibited basic Fibroblast Growth Factor (bFGF) induced endothelial cell proliferation and sprouting. In contrast, BWE stimulated fibroblast and ASC proliferation and migration. No difference was observed between cells isolated from dermis or adipose tissue. The inhibitory effect of BWE on bFGF-induced endothelial proliferation and sprouting would explain why excessive granulation tissue formation is prevented in full-thickness burn wounds as long as the eschar is still present. Identifying the eschar factors responsible for this might give indications for therapeutic targets aimed at reducing hypertrophic scar formation which is initiated by excessive granulation tissue formation once eschar is removed.",
keywords = "ASC, Burn, Endothelial cell, Fibroblast, Granulation tissue, Skin, Wound extract, Wound healing",
author = "Monsuur, {Hanneke N.} and {van den Broek}, {Lenie J.} and Jhingoerie, {Renushka L.} and Vloemans, {Adrianus F.P.M.} and Susan Gibbs",
year = "2017",
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Burn eschar stimulates fibroblast and adipose mesenchymal stromal cell proliferation and migration but inhibits endothelial cell sprouting. / Monsuur, Hanneke N.; van den Broek, Lenie J.; Jhingoerie, Renushka L.; Vloemans, Adrianus F.P.M.; Gibbs, Susan.

In: International Journal of Molecular Sciences, Vol. 18, No. 8, 1790, 18.08.2017.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Burn eschar stimulates fibroblast and adipose mesenchymal stromal cell proliferation and migration but inhibits endothelial cell sprouting

AU - Monsuur, Hanneke N.

AU - van den Broek, Lenie J.

AU - Jhingoerie, Renushka L.

AU - Vloemans, Adrianus F.P.M.

AU - Gibbs, Susan

PY - 2017/8/18

Y1 - 2017/8/18

N2 - The majority of full-thickness burn wounds heal with hypertrophic scar formation. Burn eschar most probably influences early burn wound healing, since granulation tissue only forms after escharotomy. In order to investigate the effect of burn eschar on delayed granulation tissue formation, burn wound extract (BWE) was isolated from the interface between non-viable eschar and viable tissue. The influence of BWE on the activity of endothelial cells derived from dermis and adipose tissue, dermal fibroblasts and adipose tissue-derived mesenchymal stromal cells (ASC) was determined. It was found that BWE stimulated endothelial cell inflammatory cytokine (CXCL8, IL-6 and CCL2) secretion and migration. However, BWE had no effect on endothelial cell proliferation or angiogenic sprouting. Indeed, BWE inhibited basic Fibroblast Growth Factor (bFGF) induced endothelial cell proliferation and sprouting. In contrast, BWE stimulated fibroblast and ASC proliferation and migration. No difference was observed between cells isolated from dermis or adipose tissue. The inhibitory effect of BWE on bFGF-induced endothelial proliferation and sprouting would explain why excessive granulation tissue formation is prevented in full-thickness burn wounds as long as the eschar is still present. Identifying the eschar factors responsible for this might give indications for therapeutic targets aimed at reducing hypertrophic scar formation which is initiated by excessive granulation tissue formation once eschar is removed.

AB - The majority of full-thickness burn wounds heal with hypertrophic scar formation. Burn eschar most probably influences early burn wound healing, since granulation tissue only forms after escharotomy. In order to investigate the effect of burn eschar on delayed granulation tissue formation, burn wound extract (BWE) was isolated from the interface between non-viable eschar and viable tissue. The influence of BWE on the activity of endothelial cells derived from dermis and adipose tissue, dermal fibroblasts and adipose tissue-derived mesenchymal stromal cells (ASC) was determined. It was found that BWE stimulated endothelial cell inflammatory cytokine (CXCL8, IL-6 and CCL2) secretion and migration. However, BWE had no effect on endothelial cell proliferation or angiogenic sprouting. Indeed, BWE inhibited basic Fibroblast Growth Factor (bFGF) induced endothelial cell proliferation and sprouting. In contrast, BWE stimulated fibroblast and ASC proliferation and migration. No difference was observed between cells isolated from dermis or adipose tissue. The inhibitory effect of BWE on bFGF-induced endothelial proliferation and sprouting would explain why excessive granulation tissue formation is prevented in full-thickness burn wounds as long as the eschar is still present. Identifying the eschar factors responsible for this might give indications for therapeutic targets aimed at reducing hypertrophic scar formation which is initiated by excessive granulation tissue formation once eschar is removed.

KW - ASC

KW - Burn

KW - Endothelial cell

KW - Fibroblast

KW - Granulation tissue

KW - Skin

KW - Wound extract

KW - Wound healing

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U2 - 10.3390/ijms18081790

DO - 10.3390/ijms18081790

M3 - Article

VL - 18

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1422-0067

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M1 - 1790

ER -