CD44 VARIANT ISOFORMS IN HUMAN SCAR TISSUES

瘢痕疙瘩和增生性瘢痕是创伤后异常愈合的后遗症， 口面部损伤 这些情况代表了 重塑，并与受损的功能和显着 精神障碍 它们主要是由一种异常的 细胞外基质 最近，人们发现了 在肿瘤间质的产生和伤口的愈合之间。 目的 这项初步研究的目的是调查瘢痕疙瘩是否是由于 创伤诱导的肿瘤过程或仅仅是对 损伤;这将通过研究异常瘢痕的表达来实现 CD44变体同种型的组织，肿瘤组织的已知标志物。 具体目标是：1.检查正常皮肤组织 (NSk)正常瘢痕（NSc）、增生性瘢痕（HSc）和瘢痕疙瘩（ 已知CD44亚型是肿瘤性病变的标志物。2.合成 肿瘤细胞中发现的不同CD44变体亚型的cDNA探针 病变，并使用它们来评估变体同种型基因表达。 简而言之，将从人NSk、NSc、HSc和瘢痕疙瘩获得的组织进行免疫组织化学分析。 通过免疫组织化学技术筛选CD44变体亚型 使用针对这些分子的特异性抗体。 此外， 将合成各种CD44同种型，以研究其 使用北方印迹分析和原位杂交分析这些组织的基因表达 杂交方法 这些发现将有助于了解发病机制 瘢痕疙瘩的形成，以及它是否是一个创伤引起的肿瘤过程 或是对受伤的反应 在任何一种情况下，如果CD44变体 同种型存在，并在正常的情况下差异表达。 与异常疤痕组织相比，这些结果预计将导致 使用变体特异性CD44单克隆抗体作为 开发新的诊断和治疗策略的工具 增生性疤痕和瘢痕疙瘩 最重要的是，这项工作作为 为异常瘢痕的基础生物学提供新的见解的潜力 少数民族的形成。

Keloids and hypertrophic scars are sequelae of abnormal healing after orofacial injury. These conditions represent debilitating derangements in remodeling and are associated with impaired function and significant dysmorphea. They are defined largely by an abnormal accumulation of extracellular matrix. Recently, remarkable similarities have been found between the generation of tumor stroma and the healing of wounds. The aim of this pilot study is to investigate whether keloids are the result of a trauma-induced neoplastic process or simply an inflammatory response to injury; this will be accomplished by studying expression by abnormal scar tissues of CD44 variant isoforms, known markers for neoplastic tissue. The specific aims are: 1. To survey tissues derived from normal skin (NSk), normal scar (NSc), hypertrophic scar (HSc) and keloid for variant CD44 isoforms known to be markers for neoplastic lesions. 2. To synthesize cDNA probes for the different CD44 variant isoforms found in neoplastic lesions and to use them to assess variant isoform gene expression. Briefly tissues obtained from human NSk, NSc, HSc and keloids will be screened by immunohistochemistry techniques for CD44 variant isoforms using specific antibodies against these molecules. Also, cDNA probes for the various CD44 isoforms will be synthesized, in order to study their gene expression by these tissues using Northern blot analysis and in situ hybridization. These findings will aid in understanding the pathogenesis of keloid formation and whether it is a trauma-induced neoplastic process or a reactive response to injury. In either case, if CD44 variant isoforms are present and expressed differentially in cases of normal versus abnormal scar tissues, these results are expected to lead to additional studies using variant-specific CD44 monoclonal antibodies as tools in developing new strategies for diagnosis and, perhaps, treatment of hypertrophic scars and keloids. Most importantly, this work as potential for offering new insight into the basic biology of abnormal scar formation in minorities.