CD44 VARIANT ISOFORMS IN HUMAN SCAR TISSUES

瘢痕疙瘩和增生性瘢痕是术后异常愈合的后遗症 口腔面部受伤。这些情况代表了 重塑与功能受损和显著相关 精神障碍。它们的定义在很大程度上是由 细胞外基质。最近，人们发现了显著的相似之处。 肿瘤间质的产生和伤口的愈合之间的关系。其目的是 这项初步研究的目的是调查瘢痕疙瘩是否是由 创伤诱发的肿瘤过程或仅仅是对 损伤；这将通过研究异常疤痕的表达来实现 CD44变异亚型的组织，肿瘤组织的已知标记物。 具体目的是：1.对正常皮肤组织进行观察 变异性瘢痕(NSK)、正常瘢痕(NSC)、增生性瘢痕(HSC)和瘢痕疙瘩 CD44亚型是已知的肿瘤性病变的标志。2.合成 肿瘤中发现的不同CD44异构体的cDNA探针 并用它们来评估不同亚型基因的表达。 简单地说，从人的NSK、NSC、HSC和瘢痕疙瘩中获得的组织将是 免疫组织化学技术筛选CD44变异异构体 使用针对这些分子的特定抗体。此外，还提供了一种新的 将合成各种CD44亚型，以研究它们的 Northern印迹分析和原位杂交检测这些组织的基因表达 杂交。这些发现将有助于理解其发病机制。 瘢痕疙瘩的形成以及它是否是创伤诱发的肿瘤过程 或者是对伤害的反应。在任何一种情况下，如果CD44变体 在正常情况下，异构体存在并有不同的表达。 相对于异常的疤痕组织，这些结果有望导致 使用变种特异性CD44单抗进行的其他研究 开发新的诊断和治疗策略的工具 肥大的疤痕和瘢痕疙瘩。最重要的是，它的工作方式是 为研究病理性瘢痕的基础生物学提供新的视角 在少数民族中形成队形。

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.