Genomics Study on Keloids and Hypertrophic Scars

瘢痕疙瘩和增生性疤痕的基因组学研究

基本信息

批准号：
14370574
负责人：
HYAKUSOKU Hiko
金额：
$ 7.23万
依托单位：
Nippon Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2004
项目状态：
已结题

项目摘要

We have studied and are continuing to scrutinize the cellualr and molecular mechanism of pathogenesis of keloids and hypertrophic scars to develop the effective therapeutic procedure for the scar-forming diseases. The scope of this research is also directed further to elaborate clinical diagnostic and prognostic methods, and eventually to perform scar-free surgical operations.1)Screening by using a cDNA-microarray method with 1000-probes for the gene that is known to be involved in the cell growth regulating mechanism revealed that a tumor suppressor gene, Mda-7,is expressed only in the normal control skin fibroblasts but not in keloid cells. The same cDNA-microarray showed that the expression of the thrombin receptor gene Par-1,a growth promoting factor receptor gene, is enhanced in the keloid fibroblastic cell lines. The result seemed to imply that the growth suppressor/promoter genes is implicated in the pathogenesis of keloid lesion.2)Investigation of the growth characteristics of the keloid fibroblastic cells by succesive subcultures by the 1:2-splitting procedure indicated that the cellular life span of the keloid fibroblastic cells was not different from that of the normal diploid fibroblasts.3)Although differences in the gene expression of decorin and lumican of keloid fibroblastic cells by using an oligoDNA-microarray method were detected, no significant differences in the expression of the genes were indicated between normal- and keloid-fibroblastic cells by Real-time PCR procedure.4)The independent oligoDNA-microarray assay with 20,000 probes of 5 lines of the keloid fibroblastic cells that were derived from 5 individuals with the hereditary disposition to keloids against the mixed population of 3 normal skin fibroblastic cell lines as the control revealed the keloid fibroblast specific expression of 47 genes.

我们已经研究了并继续仔细检查乳突和肥厚疤痕的发病机理的细胞和分子机制，以开发针对疤痕形成疾病的有效治疗程序。这项研究的范围还进一步针对临床诊断和预后方法，并最终执行无疤痕的手术操作。1）通过使用具有1000个基因的cDNA-微阵列方法进行筛选，该方法对基因进行了1000个探针，该基因已知与细胞的调节机制相关，表明肿瘤抑制了肿瘤的抑制作用。颅底细胞。相同的cDNA微阵列表明，在酮成纤维细胞系中，凝血酶受体基因PAR-1的表达增强了生长因子受体基因。结果似乎暗示着抑制生长抑制剂/启动子基因与乳突病变的发病机理有关。2）研究通过1：2分培养过程通过1：2分培养过程来研究毛状成纤维细胞的生长特征通过使用寡做 - 微阵列法的酮曲类成纤维细胞的装饰蛋白和腔体的表达被检测到，通过实时PCR程序在正常和酮纤维细胞之间没有明显差异。对照对照表明，针对3个正常皮肤成纤维细胞系的混合种群的乳杆状体揭示了47个基因的酮成纤维细胞特异性表达。