天津科技大学学报
天津科技大學學報
천진과기대학학보
JOURNAL OF TIANJIN UNIVERSITY OF SCIENCE & TECHNOLOGY
2015年
1期
29-33,40
,共6页
颜廷宝%廖兴华%周浩%王楠%张同存
顏廷寶%廖興華%週浩%王楠%張同存
안정보%료흥화%주호%왕남%장동존
信号转导与转录激活因子3%金属蛋白酶9%组织金属蛋白酶抑制因子1%细胞外基质%转录调节
信號轉導與轉錄激活因子3%金屬蛋白酶9%組織金屬蛋白酶抑製因子1%細胞外基質%轉錄調節
신호전도여전록격활인자3%금속단백매9%조직금속단백매억제인자1%세포외기질%전록조절
signal transducer and activator of transcription-3%matrix metalloproteinase-9%tissue inhibitor of metallopro-teinase-1%extracellular matrix%transcription regulation
通过脂质体瞬时转染Stat3重组质粒的方法在NIH3T3细胞中过表达Stat3;采用RT-PCR,Western blot以及荧光素酶活性分析的方法评估Stat3对MMP9及对其内源性抑制因子TIMP1的影响。结果表明:Stat3可增强MMP9及TIMP1基因启动子的活性,促进两者的转录与表达;并且Stat3对TIMP1的促进作用明显强于对MMP9的促进作用,从而使ECM的降解能力减弱,细胞外基质成分积累,导致纤维化的发生。
通過脂質體瞬時轉染Stat3重組質粒的方法在NIH3T3細胞中過錶達Stat3;採用RT-PCR,Western blot以及熒光素酶活性分析的方法評估Stat3對MMP9及對其內源性抑製因子TIMP1的影響。結果錶明:Stat3可增彊MMP9及TIMP1基因啟動子的活性,促進兩者的轉錄與錶達;併且Stat3對TIMP1的促進作用明顯彊于對MMP9的促進作用,從而使ECM的降解能力減弱,細胞外基質成分積纍,導緻纖維化的髮生。
통과지질체순시전염Stat3중조질립적방법재NIH3T3세포중과표체Stat3;채용RT-PCR,Western blot이급형광소매활성분석적방법평고Stat3대MMP9급대기내원성억제인자TIMP1적영향。결과표명:Stat3가증강MMP9급TIMP1기인계동자적활성,촉진량자적전록여표체;병차Stat3대TIMP1적촉진작용명현강우대MMP9적촉진작용,종이사ECM적강해능력감약,세포외기질성분적루,도치섬유화적발생。
Gene Stat3 was overexpressed in NIH3T3 cells by lipofection transfection,and the effect of Stat3 on the expres-sion of MMP9 and its inhibitor TIMP1 was estimated by RT-PCR,Western Blot and Luciferase Assay. The results show that Stat3 is able to upregulate the transcription and expression of MMP9 and TIMP1 by enhancing their promoter activities and the enhancement of TIMP1 expression induced by Stat3 is stronger than MMP9. It suggests that overexpression of Stat3 may inhibit the degradation of ECM in NIH3T3 cells and promote the development of fibrosis.