Effects of secreted apoptosis-related protein 1 on relative apoptosis proteins and apoptosis of fibroblasts in hypertrophic scar
10.3760/cma.j.issn.1671-0290.2013.06.014
- VernacularTitle:分泌型凋亡相关蛋白1调控成纤维细胞凋亡的研究
- Author:
Zhangxia REN
;
Liang CHEN
;
Xi TAO
;
Pan YU
;
Zhenxiang WANG
;
Shirong LI
- Publication Type:Journal Article
- Keywords:
Fibroblasts;
Apoptosis;
Hyperstrophic scar;
Secreted apoptosis-related protein 1 (SARP1)
- From:
Chinese Journal of Medical Aesthetics and Cosmetology
2013;19(6):445-448
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effects of secreted apoptosis-related protein 1 (SARP1) on apoptosis of the hyperstrophic scar fibroblasts (HSFB) and its regulating mechnisms.Methods The recombinant vector was identified by enzyme digestion analysis.And the virus supernatant of the recombinant vector was extracted from packaged 293 cells,then it infected the skin fibroblasts from hypertrophic scar patients,which aimed to promote its expression of SARP1 protein.After adenovirus infection,the expression of SARP1 in the fibroblasts was confirmed by RT-PCR and Western blot.The effect of SARP1 on proliferation of HSFB was detected by MTT assay,and the effect of SARP1 on apoptosis of HSFB was detected and change of the cells functions were analyzed by FACS.Results Recombinants were confirmed.After adenovirus infection,both protein and mRNA of SARP1 were detected in HSFB.And the mRNA value of SARPlwas detected to increase significantly by RT-PCR and the protein expression was detected to increase significantly by Western blot (P＜0.05).The proliferation in the groups of the adenovirus infection and HSFB was positively regulated by SARP1 (P＜0.01) and the apoptosis of them was inhibited by the expression of SARP1 as compared to the control groups of HSFB and Ad-EGFP.It showed that the apoptosis index decreased as compared the group of infected fibroblasts to the control group by flow cytometry.Conclusions SARP1 could be highly expressed in HSFB by adenovirus infection,exhibiting the proliferation-enhancing and apoptosis-inhibiting effects on HSFB.
