| Pathologic scar is a particular fibro-metabolic disease in human being. It results from wound, infection and burns etc. The mechanism of formation is very complicated. It includes hypertrophic scar(HS) and keloid(K).Both of them are similar in histology and are characterized by excessive accumulation of fibroblasts and extracellular matrix(ECM), expecially collagen. The morphologic feature of these cells are similar. Hypertrophic Scar develops in the limit of orginal wound in clinic, presses forth the normal tissue and degenerates spontaneously after growing and it's easy to contract, However, keloid is characterized by invading peripheral normal tissue and easily recurrence after resection etc. At present, pathogenesis of pathologic scar is unclear. With the rapid development of cell and molecular biology, people pay more attention to the function of apoptosis during Pathologic Scar formation. Now many scholar advance that pathologic scar could result from the lack of apoptosis and the block of apoptosis signaling. Many oncogenes have effect on the target substance of fibroblasts in pathologic scar and lead fibroblasts apoptosis to be inhibited. The research of apoptosis in tumour is more thorough, but relately behind in scars. It will provide a wide foreground to cure scars and scientific academic base to understand the mechanism of formation.Survivin effects on converged site of every apoptosis pathes and strongly represses apoptosis which were induced by overexpression of CASPASE-3 or CASPASE-7. P33ING1 regulates negatively cell growing, blocks cell in Go/Gi cycleand induce apoptosis. Cysteine aspirate protease(Caspase) is an executive for apaptosis, activates the target substance and leads DNA to break Apoptosis inhibitor Survivin and apoptosis promoter P33ING1 effect on CASPASE-3 and modulate cell apoptosis. In order to investigate the relationship between the expressions of these proteins and the formation of pathologic scar, in the present study, we detect the expressions and significance of apoptosis-derived Survivin, P33ING1, CASPASE-3 in fibroblasts derived from pathologic scar .Total 30 samples were detected by using immunnohistochemistry method, It will provide a scientific theory for clinical therapy and a new way for preventing and treating pathologic scar. Materials and methods:The tissues of pathologic scar were obtained from 30 patients who were underwent surgery; Scar tissues were collected from face, neck ,chest, shoulder abdomen and limbs. Pathologic scar were divided into two groups according to their clinical features: 1 .Hypertrophic Scar(HS): Duration: 6-24 months, hypertrophic scar remain with the boundaries of the original wound. 2.Keloid : Duration: 6-24 months, keloid extend beyond the original area of skin injury. Twenty cases of normal skin collected from patients with pathologic scar and ten cases of normotrophic scar which are charactered by no redness, pruritus, pain, and flattened with surrounded skin were used as control. Normotrophic scars were collected from face, neck and limbs. Immunohistochemical SP method and TUNEL were used to detect expressions of Survivin, P33ING1 and CASPASE-3 in pathologic scar and the two control groups, and the correlations among the expression of these proteins were systematically studied. Results:1. The positive expression of Survivin was mainly localized in the cytoplasm of fibroblasts, the positive rates in pathologic scars were 80.00% (24/30), 50.00% (5/10)> 35.00% (7/20) respectively in normotrophic scars and normal skins. The expression of Survivin were significant difference between pathologic scars group and the two control groups(p<0.05), the expression of Survivin were not significant difference between the two control groups(p>0.05)2. In normal skin group, the positive expression was mainly localized in the cytoplasm of epidermal cells,great mass of fibroblasts and part of blood vessal endodermiscell. The positive rates of P33ING1 were 43.33% (26/30), 70.00%(7/10X 85.00% (17/20) respectively in pathologic scars, normotroph...
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