Acceleration of soft tissue repair by a thrombin-derived oligopeptide.
Acceleration of soft tissue repair by a thrombin-derived oligopeptide.
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通过凝血酶衍生的寡肽加速软组织修复。
DOI：
10.1016/0022-4804(92)90022-r
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Mustoe,TA
中科院分区：
文献类型：
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作者：
Cromack,DT;Porras-Reyes,BH;Wee,SS;Glenn,KC;Purdy,JA;Carney,DH;Mustoe,TA
在软组织修复的早期阶段增强凝血酶调节的趋化性和促有丝分裂活性是可能的。凝血酶内高亲和力凝血酶受体结合结构域的鉴定使得能够合成与凝血酶受体相互作用并增强玻璃体有丝分裂的肽家族。单次（5.0 μg/伤口）应用凝血酶受体激活肽（P517-30）可显著增加第5天至第12天的伤口断裂强度（相对于对照组增加31%）。用两种放射治疗（RT）损伤愈合的模型来阐明P517- 30作用的可能机制。虽然P517- 30不能完全克服RT引起的愈合障碍，但在穿透全身RT引起的全血细胞减少和非穿透表面RT引起的真皮细胞损伤的条件下，P517- 30使断裂强度增加22%和42%。这表明P517- 30直接刺激驻留的内皮细胞、成纤维细胞或其他细胞以克服皮肤和循环单核细胞缺陷。这些结果表明了一种具有潜在临床应用的加速伤口愈合的方法，并强调了凝血酶作为生长因子的活性。
Augmentation of thrombin-modulated chemotaxis and mitogenic activity within the early phase of soft tissue repair is now possible. Identification of high-affinity thrombin receptor binding domains within thrombin has enabled the synthesis of a family of peptides which interact with thrombin receptors and enhancein vitromitogenesis. A single (5.0 μg/wound) application of the thrombin receptor-activating peptide (P517-30) significantly increased wound breaking strength from Day 5 (31% over controls) to Day 12. Two models of impaired healing created by radiotherapy (RT) were used to elucidate possible mechanisms of P517-30action. Although P517-30did not completely overcome the RT-induced healing impairments, it increased breaking strength under conditions of penetrating whole body RT-induced pancytopenia by 22% and of nonpenetrating surface RT-induced dermal cell damage by 42%. This suggests that P517-30directly stimulates resident endothelial cells, fibroblasts, or other cells to overcome dermal and circulating monocytic deficits. These results suggest a method to accelerate wound healing with potential clinical applications and emphasize the activity of thrombin as a growth factor.