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作 者:单越新[1] 罗超权[2] 徐钤[1] 利天增[3]
机构地区:[1]第一军医大学生化教研室,广州510515 [2]中山医科大学生化教研室 [3]中山医科大学第一附属医院烧伤科,广州510089
出 处:《第一军医大学学报》1999年第5期426-428,共3页Journal of First Military Medical University
摘 要:目的和方法过量Ⅰ、Ⅲ型胶原的沉积是增生性瘢痕组织和瘢痕疙瘩形成的重要原因。采用两个自行构建的SP6体外转录系统,通过掺入同位素(a32PGTP)进行放射自显影,探讨不同反义寡核苷酸对Ⅰ型胶原基因体外转录的抑制作用。结果和结论位于SP6转录起始位点区域的寡核苷酸能够有效抑制体外转录反应;而位于SP6转录起始位点下游约200bp的寡核苷酸和作为对照的随机寡核苷酸对转录的抑制作用不明显。Objective it is a very important factor that collagen type Ⅰ and type Ⅱaccumulates in excessive amount that causes theformation of keloids and hypertrophic scars. Method To understand the mechanism by which antisense oligodeoxynucleotide acts onin Vitro transcription of a1(I ) collagen gene, isotopes (a 32PGTP) was incorporated into two SP6 in vitro transcription systems.Results and conclusions Oligo-2 (at the transcription start region) could effectively inhibit in vitro transcription of pGEM3-Coll3and the control (random oligodeoxynucleotides) showed no inhibition. However, oligo-1 (at the transcription start region) obviouslyinhibited in the in vitro transcription of pGEM3-Coll4, while olig-2, which targeted the down stream region (about 200 bp) ofpromoter. showed no significant inhibition effect.
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