甘肃医药
甘肅醫藥
감숙의약
Gansu Medical Journal
2015年
1期
3-6
,共4页
转化生长因子-β1%人表皮干细胞%上皮-间质细胞转化%瘢痕
轉化生長因子-β1%人錶皮榦細胞%上皮-間質細胞轉化%瘢痕
전화생장인자-β1%인표피간세포%상피-간질세포전화%반흔
Transform growth factor-β1%Human epidermal stem cell%Epithelial-mesenchymal transformation%Scar
目的：探讨转化生长因子-β1（Transform growth factor-β1，TGF-β1）对人表皮干细胞（Human epidermal stem cell， hESCs）向间质细胞转化的影响及该现象对瘢痕增生的作用。方法：体外原代培养hESCs，分析细胞表面标志物表达，不同浓度TGF-β1刺激后，MTT 法检测细胞增殖活性，酶联免疫吸附法（ELISA）检测上皮-间质细胞转化（Epithelial-mesenchymal transformation，EMT）正相关蛋白：波形蛋白（Vimentin，Vim）、Smad3，负相关蛋白：E-钙粘着蛋白（E-cadherin，E-cad）。建立兔耳瘢痕模型，不同浓度TGF-β1干预，术后4周取材行组织形态学观察。结果：利用人包皮皮肤成功培养出hESCs，表面标记物表达阳性。不同浓度TGF-β1可促进hESCs增殖，使Vim、Smad3表达上调，E-cad表达下调，且在一定浓度范围呈剂量依赖，兔耳瘢痕标本显示各组均有瘢痕增生，TGF-β1刺激组更为明显。结论：hESCs可发生EMT现象，该现象与瘢痕增生程度一致并可被TGF-β1诱导。推测瘢痕增生的实质可能为EMT。
目的：探討轉化生長因子-β1（Transform growth factor-β1，TGF-β1）對人錶皮榦細胞（Human epidermal stem cell， hESCs）嚮間質細胞轉化的影響及該現象對瘢痕增生的作用。方法：體外原代培養hESCs，分析細胞錶麵標誌物錶達，不同濃度TGF-β1刺激後，MTT 法檢測細胞增殖活性，酶聯免疫吸附法（ELISA）檢測上皮-間質細胞轉化（Epithelial-mesenchymal transformation，EMT）正相關蛋白：波形蛋白（Vimentin，Vim）、Smad3，負相關蛋白：E-鈣粘著蛋白（E-cadherin，E-cad）。建立兔耳瘢痕模型，不同濃度TGF-β1榦預，術後4週取材行組織形態學觀察。結果：利用人包皮皮膚成功培養齣hESCs，錶麵標記物錶達暘性。不同濃度TGF-β1可促進hESCs增殖，使Vim、Smad3錶達上調，E-cad錶達下調，且在一定濃度範圍呈劑量依賴，兔耳瘢痕標本顯示各組均有瘢痕增生，TGF-β1刺激組更為明顯。結論：hESCs可髮生EMT現象，該現象與瘢痕增生程度一緻併可被TGF-β1誘導。推測瘢痕增生的實質可能為EMT。
목적：탐토전화생장인자-β1（Transform growth factor-β1，TGF-β1）대인표피간세포（Human epidermal stem cell， hESCs）향간질세포전화적영향급해현상대반흔증생적작용。방법：체외원대배양hESCs，분석세포표면표지물표체，불동농도TGF-β1자격후，MTT 법검측세포증식활성，매련면역흡부법（ELISA）검측상피-간질세포전화（Epithelial-mesenchymal transformation，EMT）정상관단백：파형단백（Vimentin，Vim）、Smad3，부상관단백：E-개점착단백（E-cadherin，E-cad）。건립토이반흔모형，불동농도TGF-β1간예，술후4주취재행조직형태학관찰。결과：이용인포피피부성공배양출hESCs，표면표기물표체양성。불동농도TGF-β1가촉진hESCs증식，사Vim、Smad3표체상조，E-cad표체하조，차재일정농도범위정제량의뢰，토이반흔표본현시각조균유반흔증생，TGF-β1자격조경위명현。결론：hESCs가발생EMT현상，해현상여반흔증생정도일치병가피TGF-β1유도。추측반흔증생적실질가능위EMT。
Objective: To explore the effect of EMT of hESCs induced by TGF-β1,and the relationship with scar hyperplasia.Methods:hESCs were primarily cultured from human foreskin,treated with different dose of TGF-β1.We detect the expression of cell surface maker,MTT and ELISA were used to detect the proliferation of hESCs and the expression of Vim、Smad3、E-cad,which were positive and negative factors of EMT respectively. Rabbit ear scar model were established and intervened with different dose of TGF-β1, the scar were obtained after 4 weeks,and were observed on histomorphology. Results:hESCs were isolated and cultured successfully, the specific marker were expressed,TGF-β1 promoted proliferation of hESCs and expression of Vim、Smad3,reduced E-cad,the changes was dose-dependent in a certain range of concentration. Animal experiment indicated that scar hyperplasia were more marked in TGF-β1 group comparing with control group. Conclusion:EMT phenomenon exists in hESCs which was consistent with the degree of scar hyperplasia,and it can be induced by TGF-β1.
