中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2010年
41期
7784-7790
,共7页
宋瑞%卞徽宁%赖文%陈德华%赵克森
宋瑞%卞徽寧%賴文%陳德華%趙剋森
송서%변휘저%뢰문%진덕화%조극삼
碱性成纤维细胞生长因子%增生性瘢痕%成纤维细胞%细胞外基质%线粒体%基因表达
堿性成纖維細胞生長因子%增生性瘢痕%成纖維細胞%細胞外基質%線粒體%基因錶達
감성성섬유세포생장인자%증생성반흔%성섬유세포%세포외기질%선립체%기인표체
背景:碱性成纤维细胞生长因子能促进愈合伤口产生胶原蛋白、纤维连接蛋白和基质酶的基质成分.然而,细胞增殖、细胞外基质及新生血管的形成或伤口基质重塑过程失调,会导致瘢痕组织过度增殖.目的:观察碱性成纤维细胞生长因子在正常皮肤创面愈合和增生性瘢痕形成中的作用.方法:从5例进行瘢痕修复手术患者身上同时取正常皮肤和增生性瘢痕组织,分离培养正常人皮肤成纤维细胞和增生性瘢痕成纤维细胞.应用RT-PCR和酶联免疫吸附法检测两种成纤维细胞胶原、纤维连接蛋白基因表达和蛋白合成.采用JC-1染色和流式细胞术测定成纤维细胞线粒体膜电位改变,采用化学发光法检测细胞内ATP水平改变.观察碱性成纤维细胞生长因子对两种细胞的上述指标的影响.结果与结论:不同浓度碱性成纤维细胞生长因子可减慢增生性瘢痕成纤维细胞生长,抑制增生性瘢痕成纤维细胞Ⅰ型胶原表达和合成(P<0.05).碱性成纤维细胞生长因子对正常皮肤和增生性瘢痕成纤维细胞Ⅲ型胶原表达和合成均无影响.然而可上调正常皮肤成纤维细胞表达纤维连接蛋白(P<0.05).此外,10,100 μg/L碱性成纤维细胞生长因子处理后增生性瘢痕成纤维细胞线粒体膜电位呈去极化趋势,正常皮肤成纤维细胞中ATP水平显著增高(P<0.05).结果表明,碱性成纤维细胞生长因子在正常皮肤创面愈合和增生性瘢痕形成中可能有不同的作用和机制.
揹景:堿性成纖維細胞生長因子能促進愈閤傷口產生膠原蛋白、纖維連接蛋白和基質酶的基質成分.然而,細胞增殖、細胞外基質及新生血管的形成或傷口基質重塑過程失調,會導緻瘢痕組織過度增殖.目的:觀察堿性成纖維細胞生長因子在正常皮膚創麵愈閤和增生性瘢痕形成中的作用.方法:從5例進行瘢痕脩複手術患者身上同時取正常皮膚和增生性瘢痕組織,分離培養正常人皮膚成纖維細胞和增生性瘢痕成纖維細胞.應用RT-PCR和酶聯免疫吸附法檢測兩種成纖維細胞膠原、纖維連接蛋白基因錶達和蛋白閤成.採用JC-1染色和流式細胞術測定成纖維細胞線粒體膜電位改變,採用化學髮光法檢測細胞內ATP水平改變.觀察堿性成纖維細胞生長因子對兩種細胞的上述指標的影響.結果與結論:不同濃度堿性成纖維細胞生長因子可減慢增生性瘢痕成纖維細胞生長,抑製增生性瘢痕成纖維細胞Ⅰ型膠原錶達和閤成(P<0.05).堿性成纖維細胞生長因子對正常皮膚和增生性瘢痕成纖維細胞Ⅲ型膠原錶達和閤成均無影響.然而可上調正常皮膚成纖維細胞錶達纖維連接蛋白(P<0.05).此外,10,100 μg/L堿性成纖維細胞生長因子處理後增生性瘢痕成纖維細胞線粒體膜電位呈去極化趨勢,正常皮膚成纖維細胞中ATP水平顯著增高(P<0.05).結果錶明,堿性成纖維細胞生長因子在正常皮膚創麵愈閤和增生性瘢痕形成中可能有不同的作用和機製.
배경:감성성섬유세포생장인자능촉진유합상구산생효원단백、섬유련접단백화기질매적기질성분.연이,세포증식、세포외기질급신생혈관적형성혹상구기질중소과정실조,회도치반흔조직과도증식.목적:관찰감성성섬유세포생장인자재정상피부창면유합화증생성반흔형성중적작용.방법:종5례진행반흔수복수술환자신상동시취정상피부화증생성반흔조직,분리배양정상인피부성섬유세포화증생성반흔성섬유세포.응용RT-PCR화매련면역흡부법검측량충성섬유세포효원、섬유련접단백기인표체화단백합성.채용JC-1염색화류식세포술측정성섬유세포선립체막전위개변,채용화학발광법검측세포내ATP수평개변.관찰감성성섬유세포생장인자대량충세포적상술지표적영향.결과여결론:불동농도감성성섬유세포생장인자가감만증생성반흔성섬유세포생장,억제증생성반흔성섬유세포Ⅰ형효원표체화합성(P<0.05).감성성섬유세포생장인자대정상피부화증생성반흔성섬유세포Ⅲ형효원표체화합성균무영향.연이가상조정상피부성섬유세포표체섬유련접단백(P<0.05).차외,10,100 μg/L감성성섬유세포생장인자처리후증생성반흔성섬유세포선립체막전위정거겁화추세,정상피부성섬유세포중ATP수평현저증고(P<0.05).결과표명,감성성섬유세포생장인자재정상피부창면유합화증생성반흔형성중가능유불동적작용화궤제.
BACKGROUND:Basic fibroblast growth factor(bFGF)can promote production of collagen,fibronectin and matrix enzyme in healing wounds.However,dysregulation of this process,such as the abnormal coordination of cell proliferation,extracellular.matrix and neovasculadzation formation,or remodeling of the wound matrix will lead to excess accumulation of scar tissues.OBJECTIVE:To investigate effects of bFGF on normal skin wound healing and hypertrophic scar formation.METHODS:Normal and hypertrophic scar fibroblasts from tissue biopsies from 5 patients who underwent plastic surgery for repairing hypertrophic scars were isolated and cultured.The expressions of collagen,fibronectin and protein synthesis were detected by RT-PCR and ELISA.The mitochonddal membrane potential changes were measured using JC-1 staining and flow cytometry.Simultaneously,adenosine tdphosphate(ATP)levels were determined by chemiluminescence method.The effects of bFGF on these indexes of normal and hypertrophic scar fibroblasts were observed.RESULTS AND CONCLUSION:Hypertrophic scar fibroblasts become slower after being exposed to bFGF,which selectively inhibited type Ⅰ collagen production in hypertrophic scar fibroblasts(P<0.05).Although bFGF inhibited type]collagen production,it had no effect on type Ⅲ collagen expression in both normal and hypertrophic scar fibroblasts.However,fibronectin expression in the normal fibroblasts was up-reguleted after bFGF treatment(P<0.05).In addition,the mitochonddal membrane potential tended to depolarization,although no statistical difference,in hypertrophic scar fibroblasts treated with bFGF(10 or 100 μg/L).bFGF treatment increased the cellular ATP levels in the normal fibroblasts,while there were no significant alterations in the hypertrophic scar fibroblasts over a treatment of bFGF(10 or 100 μg/L,P<0.05).The results suggest that there are differential effects and mechanisms on the skin fibroblasts with bFGF treatment in normal wound healing and hypertrophic scar formation.