Investigating the role of P311 in the hypertrophic scar.
The mechanisms of hypertrophic scar formation are not fully understood. We previously screened the differentially expressed genes of human hypertrophic scar tissue and identified P311 gene as upregulated. As the activities of P311 in human fibroblast function are unknown, we examined the distributio...
Main Authors: | , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2010-01-01
|
Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC2852399?pdf=render |
id |
doaj-a45589544ad744c9a0192430bc46e9cf |
---|---|
record_format |
Article |
spelling |
doaj-a45589544ad744c9a0192430bc46e9cf2020-11-24T21:49:07ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-01-0154e999510.1371/journal.pone.0009995Investigating the role of P311 in the hypertrophic scar.Jianglin TanXu PengGaoxing LuoBing MaChuan CaoWeifeng HeShunzong YuanShirong LiJohn A WilkinsJun WuThe mechanisms of hypertrophic scar formation are not fully understood. We previously screened the differentially expressed genes of human hypertrophic scar tissue and identified P311 gene as upregulated. As the activities of P311 in human fibroblast function are unknown, we examined the distribution of it and the effects of forced expression or silencing of expression of P311. P311 expression was detected in fibroblast-like cells from the hypertrophic scar of burn injury patients but not in peripheral blood mononuclear cells, bone marrow mesenchymal stem cells, epidermal cells or normal skin dermal cells. Transfection of fibroblasts with P311 gene stimulated the expression of alpha-smooth muscle actin (alpha-SMA), TGF-beta1 and alpha1(I) collagen (COL1A1), and enhanced the contraction of fibroblast populated collagen lattices (FPCL). In contrast, interference of fibroblast P311 gene expression decreased the TGF-beta1 mRNA expression and reduced the contraction of fibroblasts in FPCL. These results suggest that P311 may be involved in the pathogenesis of hypertrophic scar via induction of a myofibroblastic phenotype and of functions such as TGF-beta1 expression. P311 could be a novel target for the control of hypertrophic scar development.http://europepmc.org/articles/PMC2852399?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jianglin Tan Xu Peng Gaoxing Luo Bing Ma Chuan Cao Weifeng He Shunzong Yuan Shirong Li John A Wilkins Jun Wu |
spellingShingle |
Jianglin Tan Xu Peng Gaoxing Luo Bing Ma Chuan Cao Weifeng He Shunzong Yuan Shirong Li John A Wilkins Jun Wu Investigating the role of P311 in the hypertrophic scar. PLoS ONE |
author_facet |
Jianglin Tan Xu Peng Gaoxing Luo Bing Ma Chuan Cao Weifeng He Shunzong Yuan Shirong Li John A Wilkins Jun Wu |
author_sort |
Jianglin Tan |
title |
Investigating the role of P311 in the hypertrophic scar. |
title_short |
Investigating the role of P311 in the hypertrophic scar. |
title_full |
Investigating the role of P311 in the hypertrophic scar. |
title_fullStr |
Investigating the role of P311 in the hypertrophic scar. |
title_full_unstemmed |
Investigating the role of P311 in the hypertrophic scar. |
title_sort |
investigating the role of p311 in the hypertrophic scar. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2010-01-01 |
description |
The mechanisms of hypertrophic scar formation are not fully understood. We previously screened the differentially expressed genes of human hypertrophic scar tissue and identified P311 gene as upregulated. As the activities of P311 in human fibroblast function are unknown, we examined the distribution of it and the effects of forced expression or silencing of expression of P311. P311 expression was detected in fibroblast-like cells from the hypertrophic scar of burn injury patients but not in peripheral blood mononuclear cells, bone marrow mesenchymal stem cells, epidermal cells or normal skin dermal cells. Transfection of fibroblasts with P311 gene stimulated the expression of alpha-smooth muscle actin (alpha-SMA), TGF-beta1 and alpha1(I) collagen (COL1A1), and enhanced the contraction of fibroblast populated collagen lattices (FPCL). In contrast, interference of fibroblast P311 gene expression decreased the TGF-beta1 mRNA expression and reduced the contraction of fibroblasts in FPCL. These results suggest that P311 may be involved in the pathogenesis of hypertrophic scar via induction of a myofibroblastic phenotype and of functions such as TGF-beta1 expression. P311 could be a novel target for the control of hypertrophic scar development. |
url |
http://europepmc.org/articles/PMC2852399?pdf=render |
work_keys_str_mv |
AT jianglintan investigatingtheroleofp311inthehypertrophicscar AT xupeng investigatingtheroleofp311inthehypertrophicscar AT gaoxingluo investigatingtheroleofp311inthehypertrophicscar AT bingma investigatingtheroleofp311inthehypertrophicscar AT chuancao investigatingtheroleofp311inthehypertrophicscar AT weifenghe investigatingtheroleofp311inthehypertrophicscar AT shunzongyuan investigatingtheroleofp311inthehypertrophicscar AT shirongli investigatingtheroleofp311inthehypertrophicscar AT johnawilkins investigatingtheroleofp311inthehypertrophicscar AT junwu investigatingtheroleofp311inthehypertrophicscar |
_version_ |
1725889423670771712 |