Haifa, Israel From the Cardiovascular Research Laboratory and the Skin Research Laboratory, Bruce and Ruth Rappaport Faculty of Medicine, Technion-Israel Institute of Technology; and the Department of Plastic and Reconstructive Surgery and the Thrombosis and Hemostasis Unit, Rambam Health Care Campus.
Plast Reconstr Surg. 2013 Aug;132(2):239e-250e. doi: 10.1097/PRS.0b013e31829587e9.
Stromal cell-derived factor-1α is a chemokine and mediates endothelial progenitor cell-induced neovascularization. Because vascularization of a graft is crucial for its survival, the authors investigated whether stromal cell-derived factor-1α could improve fat graft survival by inducing endothelial progenitor cell-mediated neovascularization and preventing its resorption.
The authors injected 1 ml of human fat tissue into the scalps of 30 diabetic and 10 nondiabetic immunocompromised mice. The fat grafts were treated with phosphate-buffered saline or stromal cell-derived factor-1α. Determination of graft phenotype included measurements of their weights and volumes, vascular endothelial growth factor (VEGF) levels, the stromal cell-derived factor-1α receptor CXCR4, VEGF receptor 2, endothelial nitric oxide synthase, serine/threonine-specific protein kinase (protein kinase B), caspase 3, and cytochrome c expression levels, and the extent of vascularization.
Eighteen days after transplantation, stromal cell-derived factor-1α treatment of the grafts in the diabetic mice (1) increased plasma VEGF levels; (2) raised VEGF receptor 2, CXCR4, endothelial nitric oxide synthase, and protein kinase B expression levels; and (3) reduced caspase 3 and cytochrome c expression levels in the fat grafts. Fifteen weeks after transplantation, stromal cell-derived factor-1α treatment of the grafts prevented their resorption and increased the extent of their vascularization.
Locally delivered stromal cell-derived factor-1α increases fat graft survival by stimulating neovascularization and reducing fat cell apoptosis through an endothelial progenitor cell-mediated mechanism.
基质细胞衍生因子-1α 是一种趋化因子，可介导内皮祖细胞诱导的血管生成。由于移植物的血管化对于其存活至关重要，作者研究了基质细胞衍生因子-1α 是否可以通过诱导内皮祖细胞介导的血管生成和防止其吸收来改善脂肪移植物的存活率。
作者将 1ml 人脂肪组织注入 30 只糖尿病和 10 只非糖尿病免疫功能低下的小鼠的头皮中。用磷酸盐缓冲液或基质细胞衍生因子-1α 处理脂肪移植物。确定移植物表型包括测量其重量和体积、血管内皮生长因子 (VEGF) 水平、基质细胞衍生因子-1α 受体 CXCR4、VEGF 受体 2、内皮型一氧化氮合酶、丝氨酸/苏氨酸特异性蛋白激酶（蛋白激酶 B）、半胱天冬酶 3 和细胞色素 c 的表达水平，以及血管化的程度。
移植后 18 天，基质细胞衍生因子-1α 处理糖尿病小鼠的移植物（1）增加了血浆 VEGF 水平；(2) 提高了 VEGF 受体 2、CXCR4、内皮型一氧化氮合酶和蛋白激酶 B 的表达水平；(3) 降低了脂肪移植物中的半胱天冬酶 3 和细胞色素 c 的表达水平。移植后 15 周，基质细胞衍生因子-1α 处理移植物可防止其吸收并增加其血管化程度。
局部给予基质细胞衍生因子-1α 通过刺激血管生成和减少脂肪细胞凋亡，通过内皮祖细胞介导的机制增加脂肪移植物的存活率。
