确定BM-MSCs旁分泌作用促进体表缺血组织成活的关键蛋白

Many researchers confirmed that bone marrow mesenchymal stem cells(MSCs) can take positive effects on some ischemic diseases, such as myocardial infarction. The mechanism is unclear. Recent researches showed paracrine effects of MSCs are potential core factors to treat ischemic diseases, not differential effects of MSCs. However, key factors and key functional proteins are unclear, because of very complicated paracrine mechanism effects of MSCs. Ischemia and necrosis of superficial soft tissues are common and difficult problems in Traumatic, Plastic and Reconstructive Surgery. Surgeons usually defect effective measures to control these problems. Researches from internal ischemic diseases ignite that MSCs are possible technique to cure ischemia and necrosis of superficial soft tissues. There are rare correlation researches in field of Plastic and Reconstructive Surgery. Our preliminary experiments showed that MSCs can rescue ischemic superficial soft tissue, and found that paracrine effects of MSCs are probable key factor. Furthermore, some interesting results of researches were found in our preliminary experiments. Therefore, we present this National Science Foundation proposal for further researches. We will use McFarlane ischemic flap model in rats. We plan to adopt Differential Proteomcis Analysis as important experimental tools to find key functional proteins in paracrine effects of MSCs. as a result, the key factors for ischemic soft tissues will be make sure. Further researches and other researchers will be continued basis on our results.

大量研究证实骨髓间充质干细胞（MSCs）对于心肌梗死等缺血性疾病的积极作用，具体机制不明，故将MSCs应用于临床的报道效果也不一。最新的研究表明MSCs治疗心梗等缺血性疾病的核心作用并非直接的细胞分化，而是其旁分泌效应。但未发现MSCs复杂旁分泌效应中的关键因子。软组织缺血坏死是创伤、整形修复重建外科临床中最常见、最头痛的问题，并缺乏有效的应对手段。来自于心、脑、肾等方面的研究提示，MSCs可能是最具前景的治疗体表组织缺血坏死的方法，但本领域极少有此类研究。申请者的前期研究证实：MSCs可有效促进体表缺血组织成活，作用机制也指向旁分泌；并发现了不同于内脏缺血疾病的有趣的研究现象。故拟针对MSCs促进体表缺血组织成活，以大鼠的McFarlane缺血皮瓣为缺血组织动物模型，采用差异蛋白质组学方法，分析MSCs挽救缺血组织的旁分泌机制的差异蛋白质组学变化，确定关键蛋白点，为后续研究奠定基础。

大量研究证实骨髓间充质干细胞（MSCs）对于心肌梗死等缺血性疾病的积极作用，具体机制不明，故将MSCs应用于临床的报道效果也不一。最新的研究表明MSCs治疗心梗等缺血性疾病的核心作用并非直接的细胞分化，而是其旁分泌效应。但未发现MSCs复杂旁分泌效应中的关键因子。软组织缺血坏死是创伤、整形修复重建外科临床中最常见、最头痛的问题，并缺乏有效的应对手段。来自于心、脑、肾等方面的研究提示，MSCs可能是最具前景的治疗体表组织缺血坏死的方法，但本领域极少有此类研究。申请者的前期研究证实：MSCs可有效促进体表缺血组织成活，作用机制也指向旁分泌；并发现了不同于内脏缺血疾病的有趣的研究现象。故拟针对MSCs促进体表缺血组织成活，以大鼠的McFarlane缺血皮瓣为缺血组织动物模型，采用差异蛋白质组学方法，分析MSCs挽救缺血组织的旁分泌机制的差异蛋白质组学变化，确定关键蛋白点，为后续研究奠定基础。