Dissertation > Medicine, health > Surgery > Plastic Surgery (repair surgery ) > Plastic surgery school

Expression of Related Profibrotic Cytokine Receptors in Keloids

Author ChenXiaoDong
Tutor YeShunZhang;ZhangGuoCheng;FangFang
School Peking Union Medical College , China
Course Dermatology and Venereology
Keywords keloid transforming growth factor-beta receptor fibroblasts keloid platelet-derived growth factor receptor insulin-like growth factor-I receptor thymidine phosphorylase (TP) 5-FU MTT assay thymidine phosphorylase(TP) connective growth factor (CTGF)
CLC R622
Type PhD thesis
Year 2002
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Keloids represent a pathological response to cutaneous injury, creating disfiguring scars without known satisfactory treatment. Keloids are characterized by overabundant extracellular matrix (ECM) deposition, especially collagen. In this study, based on dermal fibroblasts which are especially thought to be responsible for the increased matrix production, we investigated the expression of some profibrotic cytokine receptors, angiogenic thymidine phosphorylase and connective growth factor which may possess therapeutic potential in keloid' dissertation">keloids compared with normal skins. This study was divided into three parts.Part I : Investigation on the expression of related profibrotic cytokine receptors in keloidsWe selected three representative profibrotic cytokines, ie transforming growth factor-beta (TGF- β ), platelet-derived growth factor (PDGF), insulin-like growth factor- I (IGF- I ). The expression of their receptors was detected by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry technique, and Western blot. Among all the two couples (T P R I and II, PDGFR- α and - β ) and a single receptor (IGF-I R ), the expression of T β RII and PDGFR- P were elevated in keloid tissues. However, T P R I , both at protein and mRNA level, was not amplified in keloids. The expression of PDGFR- α in keloid tissue seemed to be related to the state of clinical encroachment. In lesions with redness and invasiveness strong expression of PDGFR-α were observed, whereas in lesions with a stable margin PDDFR-α showed mild expression. Keloid derived fibroblasts showed significantly higher expression of T P RII, PDGFR-α and -β than normal fibroblasts. In contrast, there was no difference of the expression of T β R I and IGF-I R between keloid fibroblasts and normal controls. These findings demonstrate that,

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