SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.

Hypertrophic scars (HS) are skin disorders which occur after wounding and thermal injury. Our previous studies have suggested that secreted frizzled-related protein 2 (SFRP2) is involved in HS formation and that the suppression of SFRP2 promotes apoptosis of hypertrophic scar fibroblasts (HSFBs). Ho...

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Autores principales:	Liang Chen, Zhenxiang Wang, Shirong Li, Guangjian Zhao, Maosheng Tian, Zhicheng Sun
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/da4d905793a4410fa47aa50fe59f6deb
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spelling	oai:doaj.org-article:da4d905793a4410fa47aa50fe59f6deb2021-11-18T08:06:27ZSFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.1932-620310.1371/journal.pone.0050229https://doaj.org/article/da4d905793a4410fa47aa50fe59f6deb2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23226515/?tool=EBIhttps://doaj.org/toc/1932-6203Hypertrophic scars (HS) are skin disorders which occur after wounding and thermal injury. Our previous studies have suggested that secreted frizzled-related protein 2 (SFRP2) is involved in HS formation and that the suppression of SFRP2 promotes apoptosis of hypertrophic scar fibroblasts (HSFBs). However, the mechanisms have not been clarified. Previous studies revealed that Slug expression inhibits cell apoptosis, in vitro and in vivo, and SFRP2 regulates the expression of Slug in cervical cancer cells. In the present study, we quantified differential expression levels of expression of SFRP2 and Slug in HS and normal skin tissues by immunohistochemistry, both of which have important anti-apoptosis roles. Furthermore, a short hairpin RNA approach was adopted to investigate the potential function of SFRP2 and Slug in HSFB apoptosis. Cell apoptosis was detected using fluorescence-activated cell sorting and Caspase-3 activity was assayed by spectrophotometry. This study demonstrates that SFRP2 expression, as well as Slug, is dramatically up-regulated in HS relative to normal skin tissues, and the Slug expression is positively correlated with SFRP2. Slug expression was down-regulated in SFRP2-deficient cells, and the down-regulation of Slug expression increased sensitivity to apoptosis which was induced through a caspase-3-dependent pathway. The infected cells with reduced levels of Slug were tested for the expression of apoptosis-related genes (Bcl-2, Bax and PUMA) which were previously identified as Slug targets. Bcl-2 expression was down-regulated in Slug-deficient cells. In conclusion, SFRP2 appears to interact with Slug to affect the apoptosis of hypertrophic scar fibroblasts.Liang ChenZhenxiang WangShirong LiGuangjian ZhaoMaosheng TianZhicheng SunPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 12, p e50229 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Liang Chen Zhenxiang Wang Shirong Li Guangjian Zhao Maosheng Tian Zhicheng Sun SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
description	Hypertrophic scars (HS) are skin disorders which occur after wounding and thermal injury. Our previous studies have suggested that secreted frizzled-related protein 2 (SFRP2) is involved in HS formation and that the suppression of SFRP2 promotes apoptosis of hypertrophic scar fibroblasts (HSFBs). However, the mechanisms have not been clarified. Previous studies revealed that Slug expression inhibits cell apoptosis, in vitro and in vivo, and SFRP2 regulates the expression of Slug in cervical cancer cells. In the present study, we quantified differential expression levels of expression of SFRP2 and Slug in HS and normal skin tissues by immunohistochemistry, both of which have important anti-apoptosis roles. Furthermore, a short hairpin RNA approach was adopted to investigate the potential function of SFRP2 and Slug in HSFB apoptosis. Cell apoptosis was detected using fluorescence-activated cell sorting and Caspase-3 activity was assayed by spectrophotometry. This study demonstrates that SFRP2 expression, as well as Slug, is dramatically up-regulated in HS relative to normal skin tissues, and the Slug expression is positively correlated with SFRP2. Slug expression was down-regulated in SFRP2-deficient cells, and the down-regulation of Slug expression increased sensitivity to apoptosis which was induced through a caspase-3-dependent pathway. The infected cells with reduced levels of Slug were tested for the expression of apoptosis-related genes (Bcl-2, Bax and PUMA) which were previously identified as Slug targets. Bcl-2 expression was down-regulated in Slug-deficient cells. In conclusion, SFRP2 appears to interact with Slug to affect the apoptosis of hypertrophic scar fibroblasts.
format	article
author	Liang Chen Zhenxiang Wang Shirong Li Guangjian Zhao Maosheng Tian Zhicheng Sun
author_facet	Liang Chen Zhenxiang Wang Shirong Li Guangjian Zhao Maosheng Tian Zhicheng Sun
author_sort	Liang Chen
title	SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
title_short	SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
title_full	SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
title_fullStr	SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
title_full_unstemmed	SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
title_sort	sfrp2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/da4d905793a4410fa47aa50fe59f6deb
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SFRP2 and slug contribute to cellular resistance to apoptosis in hypertrophic scars.

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