机构地区:[1]广东医学院整形外科研究所,广东省湛江市524001
出 处:《中国组织工程研究与临床康复》2009年第28期5523-5526,共4页Journal of Clinical Rehabilitative Tissue Engineering Research
基 金:国家自然科学基金项目(30271344);广东省自然科学基金项目(020558);广东省社会发展领域科技计划项目(83034)~~
摘 要:背景:近年来临床遗传学和分子生物学研究均表明,瘢痕疙瘩的形成与遗传具有密切的关系,但增生性瘢痕与遗传是否有关,目前尚未明确。目的:了解增生性瘢痕与瘢痕疙瘩在遗传学改变上的异同。设计、时间及地点:对比观察,实验于2007-03/2008-12在广东医学院完成。材料:瘢痕标本均来自2003-01/2008-12广东医学院附属医院整形外科门诊及住院患者16例,其中增生性瘢痕10例,男3例,女7例,年龄20~50岁;瘢痕疙瘩6例,男1例,女5例,年龄19~46岁。方法:提取瘢痕疙瘩及增生性瘢痕组织DNA,应用比较基因组杂交技术观察增生性瘢痕及瘢痕疙瘩基因组的不平衡即遗传物质的丢失或扩增情况,比较两者间DNA拷贝数变化的差异。主要观察指标:①两组DNA拷贝数的缺失率的比较。②两组DNA拷贝数的扩增率的比较。结果:增生性瘢痕组未发现特异区域的DNA拷贝数的高频率缺失或扩增;瘢痕疙瘩组出现高频率的DNA拷贝数缺失的染色体是1,16,20号及22号染色体,未发现特异区域的DNA拷贝数的高频率扩增。两组1,16,20,22染色体DNA拷贝数的缺失率相比较,瘢痕疙瘩组明显高于增生性瘢痕组(P<0.05)。结论:与瘢痕疙瘩相比,增生性瘢痕不存在明显的DNA拷贝数缺失或扩增,增生性瘢痕的形成与发展可能与遗传没有直接的关系。BACKGROUND: Clinical genetics and molecular biology studies have shown that the occurrence and development of the keloid is closely related to the inheritance. However, it remians unclear if the same is ture to the hypertrophic scar. OBJECTIVE: To investigate similarities and differences of genetic alteration between the hyperplastic scar and the keloid. DESIGN, TIME AND SETTING: A contrast observational experiment was performed in Guangdong Medical College between March 2007 and December 2008. MATERIALS: Scar samples were taken from 16 patients (in-patient and out-patient) in the Department of Plastic Surgery, the Affiliated Hospital of Guangdong Medical College, with10 patients with hypertrophic scars (3 males and 7 females, 20 50 years old) and 6 patients with keloids (1 males and 5 females, 19-46 years old). METHODS: The DNA of both hyperplastic scar and keloid tissues was extracted to investigate, using comparative genomic hybridization technique, the genomic imbalance (the lose or amplification of genetic material), so as to make a comparative study on differences of the DNA copy number changes between the two. MAIN OUTCOME MEASURES: (1)Comparison on the lose rate of DNA copy number between the hyperplastic scar and the keloid. (2)Comparison on the amplification rate of DNA copy number between the hyperplastic scar and the keloid. RESULTS: Neither altofrequent loss nor amplification of DNA copy number was found in any specific DNA region of hyperplastic scar tissues; as for the keloid, special DNA altofrequent loss regions were also not found, but altofrequent DNA copy number loss regions presented in 1, 16, 20 and 22 chromosomes. Comparatively, the keloid presented much higher loss rate of the DNA copy number in 1,16,20 and 22 chromosomes than the hyperplastic scar (P 〈 0.05). CONCLUSION: The hyperplastic scar has no conspicuous DNA copy number lose or amplification compared with the keloid, which indicates that the occurrence and development of the hyperplasti
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